NUR1112 Heart Lectures 2024 PDF

http://www.toonpool.com/cartoons/heart_19057 Heart Anatomy & Physiology NUR1112 Fundamental Skills and Knowledge for Nursing and Midwifery Practice 1  Lectures prepared and delivered by Dr Natalie Bennett Unless otherwise stated, a...

http://www.toonpool.com/cartoons/heart_19057 Heart Anatomy & Physiology NUR1112 Fundamental Skills and Knowledge for Nursing and Midwifery Practice 1  Lectures prepared and delivered by Dr Natalie Bennett Unless otherwise stated, all images are the property of Pearson Education Limited and are sourced from: Marieb & Hoehn, Human Anatomy & Physiology, 10th ed., 2016 and Martini, Ober & Nath, Visual Anatomy & Physiology, 2011 Warning: This material has been reproduced and communicated to you by or on behalf of Monash University under Part VB of the Copyright Act 1968 (the Act). The material in this communication may be subject to copyright under the Act. Any further reproduction or communication of this material by you may be the subject of copyright protection under the Act. Do not remove this notice. Why is this important? ¡ This module is foundational for informed clinical practice ¡ Assessment of cardiac function is an integral part of care for all patients ¡ Cardiac function is a crucial determinant of a patient’s abilities and limitations ¡ Understanding the anatomy and physiology of the heart is crucial for the appropriate treatment of heart disease Key concepts ¡ The heart is a double pump simultaneously supplying both the pulmonary and systemic circuits ¡ Cardiac structure Pulmonary Circuit Systemic Circuit facilitates function, i.e. one-way blood flow The right atrium The left atrium collects blood from receives blood the pulmonary ¡ The cardiac cycle is a from the systemic circuit and passes circuit and empties it into the left series of continually it to the right ventricle, which ventricle, which repeated mechanical pumps blood into pumps blood into the systemic circuit. the pulmonary (muscle contraction) circuit. Systemic Circuit events ¡ The purpose of the cardiovascular system is: To provide adequate blood flow to all tissues/organs according to their immediate needs Learning Objectives 1. Describe the anatomy of the heart, including the coronary circulation 2. Describe the unidirectional pathway of blood flow through the heart. 3. Describe and explain the events of the cardiac cycle. 4. Examine the intrinsic and extrinsic innervation of the heart and explain their respective functions. 5. Define cardiac output and identify the factors that determine cardiac output.  Learning Objective 1 Describe the anatomy of the heart, including the coronary circulation Size of the heart Cone-shaped, muscular organ Typically: 12-14 cm long, 9 cm wide weights 250-350 grams approx. the size of your fist Location of the heart - the mediastinum Trachea Base of heart Right lung Left lung Apex of heart Diaphragm The heart sits in the mediastinum – the cavity between the two pleural cavities and rests on the superior surface of the diaphragm. https://upload.wikimedia.org/wikipedia/commons/thumb/5/54/2002_CPR_Technique.jpg/290px- 2002_CPR_Technique.jpg Position of the heart Base posterior to the costal cartilage of the 2nd-3rd ribs, Midline points towards right shoulder 1 1 2 2 Sternum The heart lies posterior to 3 3 the sternum and anterior 4 to the vertebral column 4 5 5 6 6 7 7 Apex typically located in 8 8 5th intercostal space, 12-14 9 10 9 10 cm below base, pointing inferiorly towards left hip  Coverings of the heart Cut edge of parietal pericardium Parietal pericardium - outer fibrous tissue Pericardial cavity containing - inner epithelial tissue pericardial fluid that produces pericardial fluid Fibrous attachment Cut edge of to diaphragm visceral pericardium OR epicardium Coverings of the heart Pulmonary trunk Fibrous layer Parietal Epithelial layer pericardium Pericardial cavity Epicardium (visceral layer of pericardium) Heart Myocardium wall Endocardium Heart chamber “Epicardium” Where the parietal pericardium meets the large blood vessels “Pericardial attached to the base of the cavity” “Heart” heart, the epithelial layer turns to “Parietal cover the heart itself, forming pericardium” the epicardium Balloon Components of the heart wall Pericardial cavity (contains pericardial fluid) Fibrous layer Parietal Epithelial layer pericardium Epicardium Myocardium Endocardium Epicardium (or visceral pericardium) – the outermost layer of epithelial tissue Myocardium - the middle layer of of cardiac muscle cells Endocardium - the inner layer of endothelial cells (flattened epithelial cells) External anatomy – anterior view Aortic arch Ascending aorta Superior vena cava Pulmonary trunk Auricle Auricle of left atrium Right atrium Fat (lying under the epicardium) Right ventricle Left ventricle Coronary sulcus Anterior interventricular sulcus External anatomy – posterior view Aortic arch Left pulmonary artery Right pulmonary Left pulmonary veins artery Fat in coronary Left Superior vena cava sulcus atrium Right pulmonary Coronary veins (superior sinus Right and inferior) atrium Left ventricle Right Inferior vena cava ventricle Posterior interventricular sulcus  Internal anatomy Aortic Ascending arch Superior aorta Pulmonary vena cava trunk Left Atrium Right Atrium Left pulmonary veins Opening of the coronary sinus Thick wall of left ventricle Right Ventricle Left Ventricle Right atrioventricular (AV) valve (tricuspid valve) Left atrioventricular (AV) valve (bicuspid or Chordae tendineae mitral valve) Papillary muscle Aortic valve (aortic Pulmonary valve semilunar valve) (pulmonary Interventricular Trabeculae carneae semilunar valve) septum (wall) Inferior vena cava Internal anatomy The difference in thickness reflects Left ventricle wall the difference in ~ 15 mm thick workload of each Right ventricle wall chamber – the left ~ 5 mm thick side must generate 4-6 times more pressure to push blood through the systemic circuit Interventricular compared to the septum (wall) ~ 15 mm thick right side and the pulmonary circuit. Transverse section of the ventricles Heart valves – atrioventricular (AV) Atrium Atrioventricular valve – pressure of incoming blood opens valve, blood moves into ventricle Chordae tendineae (loose) Papillary muscle (relaxed) AV valves open when atrial pressure > ventricular pressure Atrium Atrioventricular valve – when ventricles contract blood moves upward, pressure increases, thus valve closes Chordae tendineae (tense to prevent eversion of valve into atria and backflow of blood) Papillary muscle (contracted to tense chordae tendineae) AV valves close when atrial pressure < ventricular pressure Heart valves – semilunar (SL) Semi-lunar valves open when ventricular pressure > arterial pressure Semi-lunar valves open when the ventricles contract and push blood against the valves Semi-lunar valves close when arterial pressure > ventricular pressure Semi-lunar valves close when ventricles relax and blood in the arteries attempts to move backwards and is caught in the cusps of the valves  Heart valves – summary High pressure in the ventricle causes blood flow that pushes the Pressure from aortic valve open. the blood flowing Pressure from the blood backward in the in the left atrium pushes High pressure in the aorta closes the the mitral valve open, ventricle pushes the aortic valve. allowing blood in the blood up to the mitral left atrium to drain into valve, closing it. the relaxed ventricle. Aorta Left atrium Aortic Mitral valve Aortic valve valve (open) Mitral valve (open) (closed) (closed) Papillary muscle Left ventricle Left ventricle (tensed) (relaxed) (contracted) (a) Relaxed left ventricle (b) Contracted left ventricle  Coronary circulation - arteries The myocardium does not receive oxygen or nutrients from the blood that passes through the heart – it needs its own blood supply... Right coronary artery in coronary sulcus Left coronary artery LA Anterior LA interventricular RA artery RA RV LV LV RV Right Posterior interventricular coronary artery artery Anterior view Posterior view Coronary circulation - arteries ¡ Right and left coronary arteries arise from base of the aorta and encircle the heart in the coronary sulcus ¡ Blood moves into the coronary arteries when the ventricles relax, in between heart beats i.e. the ventricles relax and ventricular pressure drops below arterial pressure à arterial blood flows back towards to the ventricles (down pressure gradient) à as it flows backwards within the aorta it moves into the coronary arteries ¡ Left coronary artery gives rise to the anterior interventricular artery and supplies oxygenated blood to the anterior ventricles ¡ Right coronary artery supplies the right atrium and gives rise to the posterior interventricular artery which supplies oxygenated blood to the posterior ventricles Coronary circulation - veins Great LA cardiac vein LA RA Great Coronary cardiac sinus vein RA RV LV LV RV Middle cardiac Anterior view Posterior view vein Great cardiac vein drains deoxygenated blood from the anterior ventricles Middle cardiac vein drains the posterior ventricles All veins all drain into the coronary sinus (thin-walled, expanded vein)à empties into the right atrium Coronary artery disease (CAD) ¡ CAD = coronary arteries become narrowed and hardened (less elastic) ¡ Most commonly as a result of atherosclerosis (fatty plaques occluding the arteries) ¡ Over time, reduced blood flow weakens the myocardium and contributes to heart failure Normal heart Advanced CAD  Learning Objective 2 Describe the unidirectional pathway of blood flow through the heart  Both sides of the heart pump at the same time, but let s follow one Oxygen-poor blood spurt of blood all the way through the system. Oxygen-rich blood Pulmonary Tricuspid semilunar Superior vena cava(SVC) valve valve Pulmonary Inferior vena cava(IVC) Right Right atrium ventricle trunk Coronary sinus Pulmonary arteries SVC Coronary sinus Pulmonary trunk Right Tricusp atrium id Pulmonary valve semilunar Right valve IVC ventricle Oxygen-poor blood Oxygen-poor blood is To heart returns from the body carried in two pulmonary To lungs tissues back to the heart. arteries to the lungs (pulmonary circuit) to be oxygenated. Focus Figure 18.1(Marieb & Hoehn, p 694) Systemic Pulmonary capillaries capillaries To body Oxygen-rich blood is Oxygen-rich blood delivered to the body returns to the heart To heart tissues (systemic circuit). via the four pulmonary veins. Aorta Pulmonary veins Aortic Mitral Left semilunar atrium valve valve Left ventricle Aortic semilunar Mitral Valve Left valve Left Four Aorta ventricle atrium pulmonary veins  Both sides of the heart pump at the same time, but let s follow one Oxygen-poor blood spurt of blood all the way through the system. Oxygen-rich blood Pulmonary Tricuspid semilunar Superior vena cava(SVC) Right valve Right valve Pulmonary Inferior vena cava(IVC) atrium ventricle trunk Coronary sinus Pulmonary arteries SVC Coronary sinus Pulmonary trunk Right Tricuspid atrium Pulmonary valve semilunar Right valve IVC ventricle Oxygen-poor blood Oxygen-poor blood is To heart returns from the body carried in two pulmonary To lungs tissues back to the heart. arteries to the lungs (pulmonary circuit) to be oxygenated. Systemic Pulmonary capillaries capillaries To heart returns from the body carried in two pulmonary To lungs tissues back to the heart. arteries to the lungs (pulmonary circuit) to be oxygenated. Systemic Pulmonary capillaries capillaries Oxygen-rich blood is Oxygen-rich blood To body delivered to the body returns to the heart To heart tissues (systemic circuit). via the four pulmonary veins. Aorta Pulmonary veins Aortic Left semilunar Mitral atrium valve valve Left ventricle Aortic semilunar Mitral Valve Left valve Left Four Aorta ventricle atrium pulmonary veins  Learning Objective 3 Describe and explain the events of the cardiac cycle. The cardiac cycle ¡ The pumping action of the heart involves alternating periods of contraction and relaxation that produce a series of pressure and blood volume changes in the heart chambers ¡ Systole = period of contraction à increased pressure forces blood out of chambers ¡ Diastole = period of relaxation à decreased pressure allows chambers to refill ¡ Systole and diastole are coordinated mechanical events that are triggered by electrical events (action potentials in the myocardium) Cardiac cycle events ¡ The cardiac cycle = one complete heartbeat ¡ Atrial diastole and systole ¡ Ventricular diastole and systole ¡ The sequence of events during a single heartbeat: Relaxation Atria contract Ventricles contract Relaxation (atria and ventricles (ventricles relaxed) (atria relaxed) (atria and ventricles relaxed) relaxed) Phases of the cardiac cycle ¡ The sequence of events that make up the cardiac cycle can be divided into 3 phases: Ventricular Atrial Isovolumetric Ventricular Isovolumetric Ventricular filling contraction contraction phase ejection phase relaxation filling 1 2a 2b 3 Ventricular filling Ventricular systole Early diastole (mid-to-late diastole) (atria in diastole) Phase 1: Ventricular filling: 1. All 4 chambers are relaxed; mid-late ventricular diastole Aorta (passive filling) Left atrium Aortic Left AV ¡ AV valves are open, valve (open) SL valves closed Left AV valve valve (open) ¡ blood returning to atria moves directly (closed) Aortic valve into ventricles (passive Papillary muscle filling) à fills (closed) ventricles to ~ 70-80% capacity Left Left ventricle ventricle 2. Atrial systole (contracted) (relaxed) ¡ both atria contract simultaneously, completely filling the relaxed ventricles with blood (this volume = EDV) 3. Atrial systole ends and atrial diastole begins and continues until the next cycle Ventricular Atrial filling contraction 1 (NOTE: numbered points relate to events on summary slide coming up … Ventricular filling (mid-to-late diastole) EDV explained under Learning Objective 5) Phase 2a: Ventricular systole – isovolumetric contraction 4. Ventricular systole ¡ both ventricles contract - beginning at the apex, pushing blood upwards and increasing ventricular pressure ¡ upward movement of blood and Isovolumetric Ventricular increased pressure (greater than atrial contraction phase ejection phase 2a 2b pressure) closes the AV valves (produces heart sound, S1) Ventricular systole (atria in diastole) ¡ ventricular pressure not yet great enough to open SL valves so blood cannot yet exit the ventricles = Aorta Left atrium isovolumetric contraction (“iso” = “the Aortic Left AV same”) à no change in ventricular valve valve (closed) (closed) blood volume Papillary muscle ¡ atria in diastole, AV valves closed Left ventricle (NOTE: numbered points relate to events on summary slide (contracted) coming up …) Phase 2b: Ventricular systole – ventricular ejection 5. Ventricular systole ¡ increasing force of ventricular contraction à ventricular pressure increases above arterial pressure à SL valves open Isovolumetric Ventricular contraction phase ejection phase ¡ blood ejected into aorta and 2a 2b pulmonary trunk = ventricular ejection Ventricular systole (volume ejected = SV, volume (atria in diastole) remaining = ESV) ¡ AV valves closed as ventricular Left Aorta pressure is greater than atrial pressure, Aortic atrium thus blood cannot move backwards valve (open) Left AV valve (closed) ¡ atria in diastole Papillary muscle (NOTE: numbered points relate to events on summary Left slide coming up … ventricle (contracted) SV, ESV explained under Learning Objective 5) Phase 3: Ventricular diastole (early)– isovolumetric relaxation 6. Ventricular diastole (early) ¡ ventricles relax à ventricular pressure drops below arterial pressure à arterial blood flows backwards (blood flows down a pressure gradient) à closes the SL valves Isovolumetric Ventricular (produces heart sound, S2) relaxation filling 3 1 7. Isovolumetric relaxation Early diastole ¡ as ventricular pressure is still greater than atrial pressure the AV valves are still closed, Aorta Left atrium thus blood cannot move from atria into Aortic Left AV ventricles à no change in ventricular valve valve (closed) (closed) A va blood volume Papillary muscle (clo Left 8. Ventricular diastole (mid-late) ventricle (relaxing) ¡ ventricles continue to relax à ventricular pressure drops below atrial pressure (atria (NOTE: numbered have been filling with blood returning to points relate to events the heart) à AV valves open à return to on summary slide coming up next) passive ventricular filling (Phase 1) The cardiac Start cycle summary All 4 chambers Atrial systole are relaxed Atrial diastole Ventricular and atrial diastole: 0 passive filling until msec atrial systole which completes Ventricular ventricular filling 800 systole As heart rate ­ msec 100 Two phases: msec all phases Atrial Ventricular systole – shortened, systole isovolumetric especially Cardiac contraction cycle Ventricular (phase 2a) ventricular Ventricular systole diastole diastole à ¯ (late): Ventricular Atrial diastole diastole Ventricular passive filling passive systole – filling 370 time msec ventricular ejection If HR >200 bpm Ventricular (phase 2b) à ¯ blood diastole - isovolumetric exiting heart relaxation Ventricular diastole (early) Red shading = contraction of Note: numbers myocardium NOT the presence match those on of blood) previous 4 slides Heart sounds ¡ Heartbeat = S1 and S2 = “lubb-dubb” ¡ Four heart sounds (S1-S4) ¡ “Lubb” (S1) = closure of the AV Aortic valve sounds heard in 2nd intercostal space at valves right sternal margin ¡ “Dubb” (S2) = Pulmonary valve sounds heard in 2nd closure of the SL intercostal space at left sternal margin valves ¡ Heart murmur = Mitral valve sounds heard over heart apex swishing sound as (in 5th intercostal space) in line with middle of blood backflows clavicle though an incompetent valve Tricuspid valve sounds typically heard in right sternal margin of 5th intercostal space  Another way of summarizing the cardiac cycle… 1st 2nd Heart sounds 120 Ventricular systole Pressure (mm Hg) 80 Aorta Atrial Left ventricle 40 systole Left atrium 0 120 volume (ml) Ventricular EDV SV 50 ESV AV valves Open Closed Open SL valves Closed Open Closed Notes on the Phase 1 2a 2b 3 1 next 2 slides  Phase 1 Ventricular filling 1. Atrial and ventricular diastole – AV valves open, blood moves passively from the atria into the ventricles (~ 70-80% filling occurs via passive filling) 2. Atrial systole – both atria contract simultaneously, increasing pressure in the atria and 3. pushing final 20-30% of blood into the ventricles 4. Atrial systole ends. Ventricles at the end of their diastole contain a maximum amount of blood (end-diastolic volume, EDV ) Phase 2a Ventricular systole – isovolumetric contraction 5. Ventricular systole begins. Both ventricles contract simultaneously, from the apex upwards, pushing blood up and closing the AV valves (heart sound S1 = lubb). Pressure within the ventricle increases but is not yet great enough to open SL valves à isovolumetric contraction (i.e. blood volume does not change as it cannot exit the chamber yet)  Phase 2b Ventricular systole – ventricular ejection 6. When the pressure in the ventricle exceeds that in the arteries, the SL valves open and blood moves into the aorta and pulmonary trunk = ventricular ejection 7. Ventricular ejection occurs (70-80 ml blood = stroke volume) and then pressure in the ventricles starts to drop as the blood volume decreases Phase 3 Ventricular diastole – isovolumetric relaxation 8. Ventricular diastole begins and the ventricular pressure drops below that of the great arteries, the arterial blood moves backwards (down the pressure gradient) and closes the cusps of the SL valves (heart sound S2 = dubb). 9. Blood remaining in the ventricles at the end of systole is the end systolic volume (ESV). No blood is entering the ventricles from the atria as the AV valves are still closed, this period is called isovolumetric relaxation 10. As the pressure in the ventricles drops below that of the atria (which have been passively filling), the AV valves reopen and passive filling of the ventricles occurs again (Phase 1)  Learning Objective 4 Examine the intrinsic and extrinsic innervation of the heart and explain their respective functions. Innervation of the heart ¡ The mechanical activity of the heart (i.e. muscle contraction or heart beat) always begins with electrical activity (i.e. an action potential in the myocardial cells) ¡ Myocardial activity is controlled by two separate electrical systems: 1. Intrinsic conduction system (from the inside) à myocardium is able to stimulate its own contractions 2. Extrinsic innervation (from the outside) = autonomic nervous system à modifies myocardial activity Intrinsic conduction system The myocardium includes some auto-rhythmic cells called pacemaker cells: ¡ Unstable resting membrane potential ¡ Continually depolarise to generate action potentials (AP) ¡ All cardiac muscle cells have electrical connections à an AP in pacemaker cells can be conducted to the adjacent muscle cells and so on à allows coordinated contraction of the entire myocardium The pacemaker cells form the intrinsic conduction system: 1. Sinoatrial node 2. Atrioventricular node 3. Atrioventricular bundle (bundle of His) 4. Bundle branches 5. Purkinje fibres (subendothelial conducting network)  Superior Sinoatrial (SA) node vena cava (pacemaker) depolarizes 100 Right atrium times per minute Internodal pathway à depolarisation of atrial myocardium leading to contraction Atrioventricular (AV) node depolarisation pauses for 0.1 seconds Purkinje Atrioventricular (AV) bundle fibers (Bundle of His) connects atria to ventricles Bundle branches conducts Inter- depolarization through the ventricular interventricular septum septum Purkinje fibers (sub- endocardial conducting network) depolarise the ventricular myocardium (from apex upwards) leading to contraction Notes on the following 2 slides… Sinoatrial node ¡ Right atrial wall, inferior to entry point of s. vena cava ¡ Depolarises 80-100x per minute (fastest component) ¡ Acts as pacemaker and determines heart rate (sinus rhythm) ¡ Parasympathetic NS reduces this to 75x per minute at rest Internodal pathway ¡ SA node myocardial cells depolarize the surrounding myocardial cells until all atrial myocardium is depolarized ¡ Depolarisation triggers atrial contraction Atrioventricular node ¡ At the junction between the atria and ventricles ¡ Depolarises 40-60x per minute (max. 230x per min = upper limit of heart rate) ¡ Delays depolarisation for 0.1 s while atria complete contraction ¡ Becomes the pacemaker if SA node damaged Atrioventricular bundle (bundle of His) ¡ In the upper interventricular septum ¡ Only electrical connection between the atria and ventricles ¡ Damage à heart block à neither SA or AV node can control heart rate Bundle branches (right and left) ¡ Travels in the interventricular septum to the apex of the heart Purkinje fibres (subendothelial conducting network) ¡ Penetrate ventricle walls, depolarise ventricular myocardium ¡ Depolarises 30x per minute (this heart rate is too slow for adequate CO) Amazing heart facts ¡ Because the heart contains auto- rhythmic cells, it can continue to beat even when separated from the body as long as it has a supply of oxygen http://www.youtube.com/watch?v=rZAxbAVcKR0&feature=kp Extrinsic innervation ¡ Autonomic nervous system modifies the activity of the heart (otherwise heart rate is always 100 bpm – set by the SA node) ¡ Cardiac centres in the medulla oblongata: 1. Cardioacceleratory (cardiostimulatory) centre increases BOTH heart rate and force of contraction ¡ Sympathetic input via thoracic spinal cord (T1-T3) to the ¡ SA and AV nodes, ventricular myocardium, coronary arteries (causes dilation) 2. Cardioinhibitory centre decreases heart rate ONLY ¡ Parasympathetic input via vagus nerve (CN X) to the ¡ SA and AV nodes ¡ Slows SA node to ~75 depolarisations per minute at rest  Medulla oblongata Cardioinhibitory center The vagus nerve (parasympathetic) decreases heart rate Cardioacceleratory center (Only innervates the SA and AV nodes, thus only affects heart rate) Thoracic spinal cord Sympathetic cardiac (Innervates both nerves increase heart rate nodes and the and force of contraction myocardium so affects BOTH heart rate and stroke volume) AV node SA node Parasympathetic fibers Sympathetic fibers Notes on the previous slide…  Learning Objective 5 Define cardiac output and identify the factors that determine cardiac output. NOTE: The following information is a generalisation about a healthy individual with average fitness. Cardiac output ¡ The goal of cardiovascular function is the maintenance of adequate blood flow (i.e. oxygen) to (vital) tissues/organs ¡ Oxygen demands vary (i.e. depending on whether we are at rest or active) thus blood flow must vary ¡ A measure of peripheral blood flow is cardiac output ¡ Cardiac output is the volume of blood pumped by the left (or right) ventricle in one minute Cardiac output = stroke volume x heart rate CO = SV x HR  Heart rate Stroke volume (beats per minute) (mL per beat) CARDIAC OUTPUT (mL/min or L/min) ¡ Heart rate (HR) = number of beats per minute (bpm) ¡ Stroke volume (SV) = volume of blood ejected from the left (or right) ventricle per beat (mL) ¡ Cardiac output (CO) = volume blood pumped into the systemic (or pulmonary) circuit per minute (L/min) CO x = 5250 mL/min HR SV: 70 mL/beat (5.25 L/min) 75 beats/min  Blood volume Hormones Stroke volume Blood flow patterns Contractility Plasma Electrolytes Sympathetic Venous Passive Nervous return Filling Time System EDV ESV Afterload à Preload SV ¡ SV = volume of blood pumped out of a ventricle with each beat ¡ SV = EDV - ESV ¡ End diastolic volume = the volume of blood in a ventricle at the end its relaxation period, i.e. diastole (just before it contracts) (~ 120 ml at rest) ¡ End systolic volume = the volume of blood remaining in a ventricle after it has contracted (~ 50 ml or 40% of EDV) ¡ Factors which affect EDV and/or ESV will determine SV and thus CO  Blood Hormones Factors effecting EDV volume Blood flow Contractility Plasma Electrolytes patterns Sympathetic Venous Passive Nervous return Filling Time System EDV ESV Afterload à Preload ¡ EDV is determined by: SV 1. Venous return = amount of blood returning to the heart from systemic or pulmonary circuits – depends on: ¡ Total blood volume ¡ Patterns of blood flow determined by muscle/organ activity, sympathetic activity and body position 2. Passive filling time = time both the atria and ventricles are in diastole (i.e. Phase 1) ¡ decreases as HR increases (i.e. during physical activity but ¯ filling time compensated for by ­ venous return) ¡ If HR > 200 bpm à big ¯ in passive filling time à ¯ EDV à ¯ SV and CO  Blood volume Hormones EDV determines Blood flow patterns Contractility Plasma Electrolytes Sympathetic preload Venous Passive Nervous return Filling Time System EDV ESV Afterload à Preload SV ¡ The EDV determines the preload ¡ Preload = degree the myocardium is stretched before it contracts à determines the force of ventricular myocardial contraction à determines SV à A greater EDV à increased preload (myocardial stretch) à more efficient myocardial contraction à greater the SV = Frank-Starling law of the heart, OR à MORE BLOOD IN = MORE BLOOD OUT https://www.sciencenews.org/sites/default/files/2018/12/main/articles/121418_ec_rubberband_free.jpg  Blood volume Hormones Factors affecting ESV Blood flow patterns Contractility Plasma Electrolytes Sympathetic Venous Passive Nervous return Filling Time System EDV ESV Afterload à Preload ¡ Contractility SV ¡ Amount of force produced by myocardial contraction ¡ ­ contractility à higher SV (thus lower ESV) à higher CO ¡ Contractility is increased by: ¡ Sympathetic stimulation of ventricular myocardium ¡ Hormones: adrenalin, noradrenalin, thyroxine (T4) ¡ High levels of extracellular Ca2+ ¡ Exercise (increases size of the myocardium) ¡ Contractility is decreased by: ¡ Acidosis (low ECF pH) ¡ Increased extracellular K+ levels http://sjmedia.co/wp-content/uploads/2018/06/weightlifting-clipart-cartoon-can-love-image-and-olympic-lifting.jpg Factors affecting ESV ¡ Afterload ¡ The pressure that the ventricles must overcome to open the SL valves to eject blood into the arteries (i.e. how hard the ventricles must work to eject blood) ¡ Not a major factor in determining SV in healthy people ¡ Increased by factors that restrict flow into arteries, e.g. atherosclerosis in the aorta à narrows vessel and decreases compliance (i.e. stretchability) ¡ The longer it takes for the ventricles to generate enough pressure to open the SL valves, the less time there is for blood ejection, thus ­ afterload à ¯ SV (and ­ ESV)  Another analogy … https://i.ytimg.com/vi/P4xbJch9Jm0/maxresdefault.jpg  Sympathetic Nervous Parasympathetic Heart rate System Nervous System Temperature Hormones HR Plasma ¡ Altering HR is an important short- Electrolytes term control of CO and blood Other factors pressure ¡ HR is rapidly altered to: ¡ Meet the needs of our tissues/organs, e.g. increased physical activity ¡ Compensate for changes in SV, i.e. if myocardium is damaged or blood volume reduced due to dehydration https://is2-ssl.mzstatic.com/image/thumb/Purple114/v4/cc/d8/34/ccd834e4-e222-7e43-234c-5bf49a40cf34/source/512x512bb.jpg Heart rate Bradycardia 60 bpm 100 bpm Tachycardia is a condition in indicates a which the heart Normal range of faster-than- rate is slower resting heart normal than normal. rates heart rate. ¡ Each individual has a characteristic resting heart rate that varies with age, gender, general health, physical fitness ¡ Normal range = 60 – 100 beats per minute (bpm) ¡ Average rate = 75 bpm (80 bpm) Amazing heart facts ¡A woman’s heart typically beats faster than a man’s. WHY? 76 68 beats per beats per minute minute http://hesstoytruck.com/1967-hess-tanker-truck.html  Sympathetic Nervous Parasympathetic Factors affecting HR – System Nervous System The ANS Temperature Hormones ¡ Cardiovascular centres in the medulla HR Plasma Electrolytes oblongata Other factors ¡ Receives input from: ¡ Proprioceptors – monitor movement ¡ Chemoreceptors – monitor CO2, O2 and H+ levels ¡ Baroreceptors – monitor blood pressure ¡ Autonomic output: ¡ Sympathetic from cardioacceleratory centre ¡ NA binding β1 receptors which … ¡ Speeds up depolarisation of SA and AV nodes à ­ HR ¡ Parasympathetic from cardioinhibitory centre ¡ ACh binding muscarinic receptors which … ¡ Slows depolarisation of SA and AV nodes à ¯ HR ¡ Slows depolarisation of SA node (pacemaker) from ~ 100/min to ~ 75/min at rest  Sympathetic Nervous Parasympathetic Hormones and System Nervous System temperature affect HR Temperature Hormones HR Plasma Electrolytes ¡ Adrenalin and noradrenalin Other factors ¡ Released from the adrenal medulla à­ HR ¡ Thyroxine (T4) ¡ Thyroid hormones (­ cellular metabolism) à ­ HR ¡ Body temperature ¡ Increased temperature ­ HR and vice versa ¡ Plasma electrolytes ¡ Increased extracellular Na+ or K+ à ¯ HR ¡ Increased extracellular Ca2+ à ­ HR and vice versa ¡ Age/gender/general health/physical fitness ¡ Exercise à hypertrophy (enlargement) of the myocardium à ­ SV à HR can decrease at rest and still maintain CO https://www.marqueverte.com/634-large_default/digitemp-thermometre-digital-flexible-rapide.jpg http://sjmedia.co/wp-content/uploads/2018/06/weightlifting-clipart-cartoon-can-love-image-and-olympic-lifting.jpg  Summary - factors that affect CO Blood volume Hormones Blood flow Contractility Plasma Electrolytes patterns Sympathetic Venous Passive Nervous Parasympathetic return Filling Time System Nervous System EDV Temperature ESV Afterload à Preload Hormones SV HR Plasma Electrolytes CO Other factors