Lecture 8 (Cardiovascular III) PDF

Cardiovascular III: Heart as a Pump; Blood Vessels and Blood Pressure ANSC 3080 G. Bedecarrats Learning Objectives  Describe the determinants of cardiac performance  Explain the concepts of preload and afterload  Descr...

Cardiovascular III: Heart as a Pump; Blood Vessels and Blood Pressure ANSC 3080 G. Bedecarrats Learning Objectives  Describe the determinants of cardiac performance  Explain the concepts of preload and afterload  Describe the pressure changes in the systemic circulation during a cardiac cycle  Describe the determinants of blood flow and pressure  Understand the role of baroreceptor reflexes in controlling blood pressure Events during a cardiac cycle Phase 1: refilling Phase 2: atrial contraction Phase 3: isovolumic contraction Phase 4: ventricular contraction Phase 5: isovolumic relaxation Note that on this diagram, atrial contraction (phase 2) is part of diastole while the isovolumic contraction (phase 3) and isovolumic relaxation (phase 5) are part of the systole 1  Cardiac Performance Cardiac Output Mean arterial pressure CARDIAC OUTPUT = HEART RATE x STROKE VOLUME Contraction Sympathetic strength End- nerves diastolic Parasympathetic volume Stretch (EDV) nerves Frank-Starling Regulation of Heart Rate  Denervated heart rate = pace follows the SA node intrinsic rhythm  Main control = sympathetic/adrenal medulla and parasympathetic by modulating the length of potential drift in autorhythmic cells Sympathetic + Adrenal medulla Parasympathetic + + - Heart Rate 2  Regulation of Stroke Volume  Volume of blood ejected per contraction = End-Diastolic Volume (EDV) – End-Systolic Volume (ESV)  Primary determinants  EDV = preload  Volume of blood present in the ventricles at the end of diastole  Linked to the work imposed on ventricles prior to contraction  ESV = afterload  Residual volume of blood contained in ventricle after systole Depends on the impedance to ejection of blood from ventricles Effect of Change in EDV Increase in EDV = increase in stroke volume Alters cardiac performance via the Frank Starling Law of the Heart As preload is increased, the contractility of the heart is increased increased stroke volume  stretch of cardiac muscle fibres at the end of diastole induces increase in contractility by enhancing binding of Ca++ to troponin-C Under resting condition, EDV stretches cardiac muscle to sub-optimal levels (there is room for increase) BUT: stretching the cardiac muscle beyond optimum does not occur (pericardium) Factors Affecting Preload (EDV) Main factor is the venous return Increased venous return = increased EDV Decreased venous return = decreased EDV 3  Venous Return Dependent on the pressure difference between the large veins and the right atrium Skeletal muscle pump Muscle contraction squeezes veins = push blood towards heart (valves in veins prevent backflow) Respiratory activity (respiratory pump) Inspiration (contraction of the diaphragm)  Increases abdominal pressure = transfer to abdominal veins  Creates low pressure in the thoracic cavity, where the vena cava is Blood volume Increased blood volume = elevated venous return Autonomic nervous system Veins contain smooth muscle innervated by sympathetic fibers Increase in APs in nerve fibers = contraction Increase pressure in vein Increase venous return 4 Factors Affecting Afterload (ESV)  Resistance the ventricles encounter during ejection  During exercise, indirectly controlled by the heart contractility (higher contractility = lower ESV)  Stimulated by the sympathetic nervous system  During rest, main determinant is arterial vasomotor tone (arterial vascular resistance) = Total Peripheral Resistance (TPR)  Measure blood pressure as surrogate indicator of afterload BP = cardiac output x arterial resistance Blood Pressure Blood Vessels Important factors are Diameter Elasticity Contractility 5  Some Definitions Flow = volume of fluid transported per time unit Flow between 2 points is dependent on pressure difference between the 2 points Flow between 2 points is dependent on the resistance to fluid Flow (Q) = Pressure difference (P) / Resistance (R) Pressure higher in arteries than veins Arterioles are the “bottlenecks” of the circulation Main site of pressure/flow regulation as they have the most smooth muscle Significance Important factor = (P) not total P Initial pressure results from the heart contraction Pressure progressively decreases Resistance: depends on Length of vessel (constant in an individual) Radius of vessel = most important factor Resistance decreases by the 4th power of the radius: if radius increases 2 times, resistance decreases 16 times Viscosity of blood varies with cells and proteins amount Is not the main control role Arterial Pressure During a Cardiac Cycle  When the aortic valve opens during ventricular contraction  Rapid flow of blood  Increased arterial pressure  Aorta elasticity absorbs some of the pressure (temporarily stores energy like a rubber elastic)  When the aortic valve closes during diastole  No blood flowing from the ventricle  Energy stored during the stretching of the aorta released  Allows blood flow to continue in vessels  Gradual decrease in arterial pressure 6  Arteries Arteries are compliant Elastic, large diameter = low resistance = High flow Recoil of wall limits the drop in pressure after systole  More continuous flow  However, a difference in arterial blood pressure can be observed between systole and diastole Systolic pressure Diastolic pressure Aortic Blood Pressure Profile Systole Diastole 125 Aortic Valve Closure Pressure (mm Hg) Mean Blood Pressure (MBP) 75 During rest: MBP closer to diastolic pressure Diastole last longer than systole During exercise: MBP closer to systolic pressure Heart rate increase = diastole shortened Difference between systolic and diastolic pressure = PULSE PRESSURE Measure of pressure on artery wall during systole 7 Factors Influencing Arterial Pressure  Elasticity of the artery  Low elasticity = high pressure (aging)  Cardiac output  More blood from systole = increased pressure  Respiration  During inspiration, low pressure in the thoracic cavity (low pressure around the heart and major vessels), high pressure in the abdominal cavity (promotes venous return)  During expiration, pressure increases in thoracic cavity and lower pressure in the abdominal cavity  Resistance to blood flow (main factor)  Total peripheral resistance (TPR) depends on vasoconstriction of arterioles. TPR  = pressure   Blood volume  Influences the cardiac output (minimal effect because vein absorb the major effect) Control of Vascular Resistance (Arteriolar Diameter) Arterioles’ walls have fewer elastic fibers but have larger number of smooth muscle fibers Basal level of constriction = myogenic tone (basal tone). Makes it possible to decrease and increase vessels contraction thus diameter Diameter decreases = resistance increases Two levels of control of arteriolar resistance Autoregulation (local mechanisms) Extrinsic control factor (neuro-hormonal) Autoregulation (local)  Within organ or tissue; overrides extrinsic regulation  Controls flow to critical organs (heart-coronary arteries, brain, liver, kidneys, working skeletal muscles) = protective mechanism Metabolic regulation:  Response to changes in metabolism, thus blood requirement  Results in increase in diameter (CO2, pH, K+, NO)  Relative importance of factors depend on the organ Myogenic (pressure) autoregulation:  Vessels respond to changes in tone or stretch  Maintain the blood supply virtually unchanged even when pressure changes 8  Extrinsic Regulation Regulates the peripheral pressure as a whole Vasoconstrictive influences: Sympathetic stimulation on -adrenergic receptors (remember, in the heart -adrenergic receptors) Angiotensin II (will be covered in details in urinary chapter) Arginin vasopressin Few vasodilatory influences: Parasympathetic stimulation (vagus nerve; mainly in penis and clitoris) Veins and Venous Pressure  When blood enters the venous system, pressure is as low as 10 mm Hg  Still travels towards the right atrium  P sufficient  During inspiration, P in the thoracic cavity ↓ and P in abdominal cavity ↑ (follows movement of the diaphragm)  Veins have little resistance  Heart acts as a pump  Low pressure after contraction sucks blood upward  Skeletal muscle activity can help squeeze blood upward  Veins possess smooth muscles  When pressure in veins too high: flow is reduce and fluid leaks out and accumulate in tissue (edema) Control of Blood Pressure (how it works) Main variables Heart rate Stroke volume TPR (here we are talking of extrinsic regulation) Blood pressure reflex Baroreceptors Sensory fibers Integration center Motor fibers Effectors 9  Baroreceptors: Stretch receptors: sense stretching of arterial wall Free nerve endings Located in sensitive areas: Aortic arch Carotid sinus Sensory fibers: Ascend via vagus nerve Stretch increases = increase in APs frequency Stretch decreases = decrease in APs frequency Integration center: Cardiovascular (vasomotor) center in the medulla oblongata Compares information to reference value Motor fibers: Autonomic nervous system (both branches) Effectors: Heart: rate and stroke volume = cardiac output Arterioles and vein = TPR Baroreceptors in Action….  Postural hypotension  Change from lying to standing position  Shift 500-700 ml of blood from thoracic cavity to lower extremities   venous return,  CO,  BP  [almost] immediately compensated by baroreceptor reflex   firing in stretch receptors  parasympathetic activity =  heart rate  sympathetic activity =  heart rate, stroke volume and vasoconstriction 10 Other Mechanisms of BP Control Atrial volume receptor reflex Stretch receptors in wall of atria Called volume receptors as volume of blood in atria determines atrial wall stretch Regulates blood volume via Autonomic nervous system activity (similar to baroreflex responses) Neural input that controls thirst and the secretion of hormones that alter renal handling of sodium and water Hormones and BP Regulation  Atrial natriuretic peptide (ANP)  Synthesized in atrial wall  Increases sodium excretion  Renin  Synthesized in kidney increases synthesis of angiotensin II aldosterone Angiotensin II – vasoconstriction Aldosterone – decrease sodium excretion  Antidiuretic hormone = vasopressin (post. pituitary)  Decreases water excretion (kidney) 11