CV Heart Anatomy and Coronary Circulation PDF
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This document is a presentation on the CV system. It provides a comprehensive overview of the heart's structure, including chambers, valves, and the path of blood flow. It also details the coronary circulation, potential diseases like CAD and myocardial infarction, and the functioning of cardiac muscle. Additionally, it discusses cardiac tamponade and treatment, and reviews the different pathways of blood flow through the heart and coronary circulation, and briefly contains questions.
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Valentine’s Day Quiz 1. What was the famous “first” of Dr. Christian Barnard? 2. Gastric reflux can lead to _________. 3. What is the song Tony Bennett made famous? 4. Name a song that is often in the repertoire of the beginning pianist: 5. Who said “off with her head” in Alice in Wo...
Valentine’s Day Quiz 1. What was the famous “first” of Dr. Christian Barnard? 2. Gastric reflux can lead to _________. 3. What is the song Tony Bennett made famous? 4. Name a song that is often in the repertoire of the beginning pianist: 5. Who said “off with her head” in Alice in Wonderland? 6. Name a Poe famous tale of terror…. 7. Ryan Gosling, Ryan Reynolds, Jason Derulo… 8. Dick Tracy’s girlfriend: 9. Politically motivated liberal left: 10. Card game: 11. Elvis Presley song: 12. Food category: 13. Close and personal conversation: 14. Mel Gibson movie: CV system = heart, blood vessels, and blood [heart pumps blood into blood vessels throughout the body] 4 MODULE 17.1 OVERVIEW OF THE HEART 5 Location & Structure of the Heart Heart cone-shaped organ located slightly to left side in thoracic cavity (in mediastinum) rests on diaphragm (Figure 17.1a) Apex : inferior aspect ~ 250 to 350 grams (< 1 lb.) 6 Location & Structure of the Heart Figure 17.1a Location and basic anatomy of the heart in the thoracic cavity. Location & Structure of the Heart Figure 17.1b Location and basic anatomy of the heart in the thoracic cavity. Location & Structure of the Heart Chambers and external anatomical features: Chambers – RA and LA atria (atrium) RV and LV ventricles Atrioventricular sulcus – external indentation between the atria and ventricles Interventricular sulcus – external depression between RV and LV 9 Location & Structure of the Heart Figure 17.1c Location and basic anatomy of the heart in the thoracic cavity. Location & Structure of the Heart Veins - carry blood to heart Arteries carry blood away from heart Great vessels = main veins and arteries that bring blood to and from heart [SVC, IVC, pulmonary V., pulmonary A., aorta] 11 Pulmonary & Systemic Circuits Pulmonary Circuit: Right side of heart (pulmonary pump) pumps blood to lungs – Pulmonary arteries deliver oxygen-poor (deoxygenated) blood to lungs – Gas exchange between alveoli and pulmonary capillaries – Pulmonary veins deliver oxygen-rich (oxygenated) blood to left side of heart 12 Pulmonary Circuit Figure 17.2a pulmonary and systemic circuits. Pulmonary & Systemic Circuits Systemic Circuit: Systemic pump (left side of heart) - receives oxygenated blood from pulmonary veins and pumps it to rest of body - Systemic arteries pump oxygen-rich (oxygenated) blood to all systems of body (not lungs) - Gas exchange at systemic capillaries - Systemic veins return oxygen-poor (deoxygenated) blood to RA 14 Pulmonary & Systemic Circuits Pulmonary circuit -low-pressure circuit pumps blood only to lungs Systemic circuit high-pressure circuit pumps blood to rest of body 15 Systemic Circuit Figure 17.2b pulmonary and systemic circuits. Functions of the Heart Heart helps maintain BP (blood pressure) – Rate and force of contraction influence BP and blood flow to organs Atria produce hormone: atrial natriuretic peptide (ANP) ANP lowers BP by decreasing Na+ retention in kidneys decr. osmotic H2O reabsorption 17 MODULE 17.2 HEART ANATOMY AND BLOOD FLOW PATHWAY 18 Pericardium Pericardium – membrane surrounding heart 1. Fibrous pericardium – outermost layer 2. Serous pericardium – produces serous fluid – Parietal pericardium [pericardial cavity] – Visceral pericardium – (aka epicardium) 19 Pericardium Pericardial cavity - contains serous fluid (pericardial fluid) - acts as a lubricant, decreasing friction 20 Heart Wall 1. Epicardium - outmost layer 2. Myocardium – middle muscle layer Cardiac [What type of muscle??] - fibrous skeleton (dense irregular collagenous CT) 3. Endocardium - innermost endothelial layer 21 Pericardium & Heart Wall Figure 17.3 The pericardium and the layers of the heart wall. Cardiac Tamponade (p. 635) Pericardial cavity fills with excess fluid cardiac tamponade Causes: trauma, certain cancers, kidney failure, thoracic surgery, and HIV Fibrous pericardium - strong but not very flexible, excess fluid in pericardial cavity squeezes heart; reduces filling of ventricles Treatment – remove excess fluid via needle inserted into the pericardial cavity 23 Coronary Circulation Coronary vessels (supply heart wall): Branch off ascending aorta: 1. right coronary artery post. interventricular (post. descending a. marginal branch 2. left coronary artery circumflex branch ant. interventricular a. (left ant. descending) LAD 24 Coronary Circulation Anterior Posterior Figure 17.4a The coronary circulation. Coronary Circulation Coronary veins Great cardiac vein Small cardiac vein Coronary sinus RA Middle cardiac vein Coronary Sinus 26 Coronary Circulation Coronary artery disease (CAD) – buildup of plaques (fatty material) in coronary arteries – decreases blood flow to myocardium myocardial ischemia – Symptoms: angina pectoris – leading cause of death worldwide 27 Plaque buildup in an artery Reduced flow angina Cardiac Catheterization Angioplasty & stent placement 28 Coronary Circulation Myocardial infarction (MI) or heart attack – Most dangerous potential consequence of CAD – Occurs when plaques in coronary arteries rupture - Clot forms myocardial tissue infarct - Symptoms include chest pain radiates to left arm shortness of breath, sweating, anxiety, and nausea and/or vomiting – Women may present with back, jaw, or arm pain instead 29 Coronary Circulation – Survival after MI depends on extent and location of damage – Dead cells are replaced with scar tissue – Death of part of myocardium increases workload of remaining heart muscle – Risk factors include smoking, incr. BP, poorly controlled diabetes, high levels of certain lipids, obesity 30 Coronary Circulation Angiography diagnostic test for CAD Treatments modify Lifestyle medications then invasive treatments 31 Coronary Circulation Coronary angioplasty - balloon is inflated in blocked artery and stent inserted Coronary artery bypass grafting (CABG) - other vessels are grafted onto diseased coronary artery to bypass blockage 32 Path of Blood through the Heart Heart consists of four chambers: (Figures 17.5–17.7): 2 Atria - receive blood from veins - pump through atrioventricular (AV) valves into ventricles 2 Ventricles - eject blood into arteries - carry blood through systemic or pulmonary circuit 33 Path of Blood through the Heart – Superior vena cava (SVC) – Inferior vena cava (IVC) – Coronary sinus 1. Right Atrium (RA) (tricuspid) 2. Right Ventricle (RV) chordae tendineae papillary muscles 34 Path of Blood through the Heart < Pulmonary semilunar valve> pulmonary trunk LUNGS pulmonary veins 3. Left Atrium (LA) (bicuspid or mitral) 4. Left Ventricle (LV) chordae tendineae papillary muscles 35 Path of Blood through the Heart < aortic semilunar valve > Ascending aorta: o openings to coronary arteries Aortic Arch o Brachiocephalic artery o Left common carotid (LCC) artery o Left subclavian artery 36 Great Vessels, Chambers, and Valves Figure 17.5a The external anatomy of the heart. Great Vessels, Chambers, and Valves Figure 17.5b The external anatomy of the heart. Great Vessels, Chambers, and Valves Posterior View Figure 17.5c The external anatomy of the heart. Great Vessels, Chambers, and Valves – Pectinate muscles – muscular ridges inside RA – Interatrial septum – wall between RA & LA – Fossa ovalis – indentation in interatrial septum; remnant of opening (foramen ovale) from fetal circulation – Trabeculae carneae – ridged surface in Ventricles “beams of flesh” 40 Great Vessels, Chambers, and Valves RV – low pressure LV – high pressure LV wall = 3x thicker than RV Great Vessels, Chambers, and Valves Blood Flow - heart Figure 17.6 The internal anatomy of the heart, anterior dissection. Heart Valves Tricuspid (right AV) Pulmonary semilunar Bicuspid (mitral, left AV) Aortic semilunar Heart Valves Pulmonary semilunar valve- located between RV and pulmonary trunk Figure 17.7b Anatomy of the atrioventricular and semilunar valves. The Big Picture - Blood Flow through the Heart Figure 17.8 The Big Picture of Blood Flow through the Heart. The Big Picture - Blood Flow through the Heart Figure 17.8 The Big Picture of Blood Flow through the Heart. Valvular Heart Diseases (p. 643) Diseases of heart valves - congenital (present at birth) or acquired (infection, cancer, or immune system disorder) Two major types of valvular defects: Insufficient valve – fails to close fully, blood leaks backward Stenotic valve (narrowing) – calcium deposits hard and inflexible 47 Valvular Heart Diseases Both valve disorders may cause heart murmur Symptoms: enlargement of heart, fatigue, dizziness, and heart palpitations Mitral and aortic valves are ones most commonly affected (left heart) 48 MODULE 17.3 CARDIAC MUSCLE TISSUE ANATOMY AND ELECTROPHYSIOLOGY 49 Electrophysiology Cardiac muscle exhibits autorhythmicity Cardiac muscle cells contract in response to electrical excitation in form of APs Cardiac muscle cells do not require stimulation from nervous system to generate APs 50 Electrophysiology Pacemaker cells – specialized cardiac muscle cells (=1% of cardiac muscle cells) - coordinate cardiac electrical activity - rhythmically and spontaneously generate APs to other type of cardiac muscle cell (contractile cells = 99% of cardiac muscle) 51 Histology of Cardiac Muscle Tissue and Cells Cardiac muscle cells – striated – branched, uninucleated – intercalated discs – generate tension through sliding-filament mech. Ex. of Structure-Function Core Principle 52 Histology of Cardiac Muscle Tissue and Cells Figure 17.9 Cardiac muscle cells. Histology of Cardiac Muscle Tissue and Cells Like skeletal muscle fibers, cardiac muscle cells contain selective gated ion channels Opening & closing action of these ion channels both pacemaker & contractile cardiac APs 54 Electrophysiology of Cardiac Muscle Cardiac conduction system – Pacemaker cells undergo rhythmic, spontaneous depolarizations APs Functional syncytium – Permits heart to contract as a unit and produce a coordinated heartbeat 55 Electrophysiology of Cardiac Muscle Figure 17.10 A contractile cell action potential. Electrophysiology of Cardiac Muscle Figure 17.10 A contractile cell action potential. Electrophysiology of Cardiac Muscle Sequence of events of contractile cell AP resembles that of skeletal muscle fiber AP with one exception: plateau phase Plateau phase lengthens cardiac AP slows HR providing time required for heart to fill with blood; also increases strength of heart’s contraction; prevents tetany (sustained contraction) in heart by lengthening refractory period 58 Electrophysiology of Cardiac Muscle Electrophysiology of Cardiac Muscle – Refractory period in cardiac muscle cells is so long that cells cannot maintain a sustained contraction – allows heart to relax and ventricles to refill with blood before cardiac muscle cells are stimulated to contract again 60 Cardiac conduction system: Sinoatrial node (SA node) - located in upper RA - 60 to 100 bpm influenced by SNS & PSN Atrioventricular node (AV node) - located near tricuspid valve - 40 bpm - AV node delay Purkinje fiber system 61 Electrophysiology of Cardiac Muscle Purkinje fiber system: Atrioventricular bundle (AV bundle) – Right and left bundle branches - Purkinje fibers - located in ventricular walls 62 Electrophysiology of Cardiac Muscle AV node delay - allows atria to depolarize (and contract) before ventricles, giving ventricles time to fill with blood - also helps to prevent current from flowing backward from AV bundle into AV node and atria 63 Electrophysiology of Cardiac Muscle Figure 17.12 The cardiac conduction system. Electrophysiology of Cardiac Muscle – SA node = main pacemaker of heart – Sinus rhythms = electrical rhythms generated and maintained by SA node 65 Electrophysiology of Cardiac Muscle Electrocardiogram (ECG) – graph of electrical activity in cardiac muscle cells over time (Figure 17.13) - electrodes placed on patient’s skin (6 on chest, 2 on each leg) - detects disturbance in electrical rhythm = dysrhythmia or arrhythmia (= no rhythm) 66 Electrophysiology of Cardiac Muscle – ECG represents depolarization or repolarization of parts of heart P wave represents depolarization of atria QRS complex represents ventricular depolarization T wave represents ventricular repolarization What’s missing?? Atrial repolarization – masked by QRS complex 67 Electrophysiology of Cardiac Muscle Figure 17.13 A normal electrocardiogram (ECG) tracing. Electrophysiology of Cardiac Muscle Determine HR Spread of depolar. through atria Spread of depolar. through ventricles Figure 17.13 A normal electrocardiogram (ECG) tracing. Electrophysiology of Cardiac Muscle Figure 17.13 A normal electrocardiogram (ECG) tracing. Electrophysiology of Cardiac Muscle Figure 17.13 A normal electrocardiogram (ECG) tracing. Dysrhythmias (p. 652) Cardiac dysrhythmias have 3 basic patterns: 1. Disturbances in heart rate (HR): Bradycardia = HR < 60 bpm Tachycardia = HR > 100 bpm sinus tachycardia = regular, fast rhythm 72 Dysrhythmias 2. Disturbances in conduction pathways – disrupted by accessory pathways between upper & lower chambers or by heart block – Heart block at AV node; P-R interval is longer than normal, due to incr. time for impulses to spread to ventricles through AV node; extra P waves are present, indicates that some APs from SA node are not being conducted through AV node 73 Dysrhythmias Right or left bundle branch block - generally widens QRS complex due to depolarization taking longer to spread through ventricles 74 Dysrhythmias 3. Fibrillation = electrical activity goes haywire parts of heart to depolarize and contract while others are repolarizing and not contracting - bag of worms writhing V.Fib 1min 75 V.fib. Khan Acad. 8min Dysrhythmias – Atrial fibrillation generally not life threatening atrial contraction isn’t necessary for ventricular filling ECG tracing “irregularly irregular” rhythm (one that has no discernible pattern) that lacks P waves A-Fib. 2min 76 Dysrhythmias – Ventricular fibrillation immediately life-threatening ECG exhibits chaotic activity defibrillation (an electric shock to heart) depolarizes all ventricular muscle cells simultaneously SA node will resume pacing heart after shock is delivered (ideally) 77 Dysrhythmias “Flat-lining” = asystole - defibrillation is not used for asystole because heart is not fibrillating and there is no electrical activity to reset - instead, treated with CPR and pharmacological agents that stimulate heart such as atropine and Epi 78 MODULE 17.4 MECHANICAL PHYSIOLOGY OF THE HEART: THE CARDIAC CYCLE 79 Introduction to Mechanical Physiology Mechanical physiology - actual processes by which blood fills and is pumped out of chambers Heartbeat = cardiac muscle cells contract as a unit to produce one coordinated contraction Cardiac cycle - sequence of events that take place from one heartbeat to next (systole followed diastole for each chamber) 80 Pressure Changes, Blood Flow, and Valve Function Blood flows in response to pressure gradients (Gradients Core Principle); as ventricles contract and relax, pressure in chambers changes, causing blood to push on valves and open or close them (Figure 17.14): Ventricular systole (contraction phase) – Both of AV valves are forced shut by blood pushing against them – Both of semilunar valves are forced open by outgoing blood 81 Pressure Changes, Blood Flow, and Valve Function Figure 17.14a Pressure changes, blood flow, and valve function. Pressure Changes, Blood Flow, and Valve Function Ventricular diastole (relaxation phase) – Press. In ventricles falls below those in atria and in pulmonary trunk and aorta forces AV valves open, allowing blood to drain from atria into relaxed ventricles Higher pressures in pulmonary trunk and aorta push cusps of semilunar valves closed 83 Pressure Changes, Blood Flow, and Valve Function Figure 17.14b Pressure changes, blood flow, and valve function. Pressure Changes, Blood Flow, and Valve Function Stethoscope – used to listen to (auscultate) rhythmic heart sounds (Fig. 17.15): – S1 (“lub”) = AV valves close – S2 (“dub”) = semilunar valves close Normal Heart sound Aortic stenosis -early Mitral stenosis 85 Pressure Changes, Blood Flow, and Valve Function Figure 17.15 Heart sounds. Heart Murmurs and Extra Heart Sounds (p. 654) Heart murmur - turbulent blood flow through heart often due to defective valves, defective chordae tendineae, or holes in interatrial or interventricular septum 87 Pressure Changes, Blood Flow, and Valve Function Cardiac cycle = one diastole plus one systole for each chamber of heart (Fig. 17.16, 17.17) – Cycle is divided into four main phases that are defined by actions of ventricles and positions of valves: filling, contraction, ejection, and relaxation 88 Pressure Changes, Blood Flow, and Valve Function 1. Ventricular filling phase of cardiac cycle - blood drains from atria into ventricles – Pressures in LV and RV are lower than in atria, pulmonary trunk, and aorta – Higher pressures in pulmonary trunk and aorta cause semilunar valves to be closed; prevents backflow of blood into ventricles 89 Pressure Changes, Blood Flow, and Valve Function 1.Ventricular Diastole (filling phase) Figure 17.16 Events of the cardiac cycle. Pressure Changes, Blood Flow, and Valve Function 2. Ventricular Systole (Contraction Phase) Figure 17.16 Events of the cardiac cycle. Pressure Changes, Blood Flow, and Valve Function 3. Ventricular Ejection Figure 17.16 Events of the cardiac cycle. Pressure Changes, Blood Flow, and Valve Function 4. Ventricular Relaxation (diastole) Figure 17.16 Events of the cardiac cycle. Pressure Changes, Blood Flow, and Valve Function Figure 17.16 Events of the cardiac cycle. Pressure Changes, Blood Flow, and Valve Function Figure 17.17 Comparison of pressure changes in left and right ventricles during the cardiac cycle. Pressure Changes, Blood Flow, and Valve Function ECG Heart Sounds Pressure changes Volume changes Figure 17.18 Wigger’s diagram showing an overview of electrical and mechanical events in the heart during the cardiac cycle. MODULE 17.5 CARDIAC OUTPUT AND REGULATION 97 Introduction to Cardiac Output and Regulation Heart rate (HR) = 60–80 cardiac cycles or bpm Stroke volume = ~70 ml/beat (amt. of blood ejected from each ventricle in a beat) Cardiac output (CO) = vol. of blood pumped into pulmonary & systemic circuits in 1 minute (ml/min) 98 Determination of Cardiac Output C.O. = heart rate x stroke volume: – 72 beats/min × 70 ml/beat = 5040 ml/min ~5 liters/min (C.O.) – Resting C.O. ~ averages about 5 liters/min; RV pumps ~ 5 liters into pulmonary circuit LV pumps same amt. to systemic circuit Normal adult blood volume = ~ 5 liters [:. entire supply of blood supply passes through heart each minute] 99 Factors that Influence Stroke Volume Frank-Starling law Increased ventricular muscle cells stretch, leads to forceful contraction Ensures that vol. of blood discharged from heart is equal to vol. that enters it Important during exercise, when C.O. must increase to meet body’s needs 100 How Changes in Preload, Contractility, and Afterload Affect Stroke Volume Factors that determine stroke volume—preload, contractility, and afterload— illustrated using only the left ventricle for simplicity. 101 Ventricular Hypertrophy (p. 662) Long-standing increases in preload and afterload are associated with enlargement of ventricles (ventricular hypertrophy) Cardiac muscle cells of ventricles need to generate more tension to continue pumping blood against higher afterload; cells respond same as skeletal muscle fibers when they have to generate more tension—they make more myofibrils and more organelles, and as a result they get bigger 102 Ventricular Hypertrophy - Right ventricular hypertrophy most often results from respiratory disease or high blood pressure in pulmonary circuit; left ventricular hypertrophy generally results from high blood pressure in systemic circuit Ventricular hypertrophy can increase effectiveness of heart’s pumping up to a certain point; condition decreases heart lumen and so filling space Increases risk for many other cardiac conditions, including heart failure 103 Factors that Influence Heart Rate HR due to rate at which SA node generates APs Factors that influence rate at which SA node depolarizes = chronotropic agents Positive chronotropic agents – SNS, some hormones, increased body temp. Negative chronotropic agents - PSN, decreased body temperature 104 Regulation of Cardiac Output Heart is autorhythmic but still requires regulation to ensure C.O. meets body’s needs at all times Regulated by nervous (ANS) and endocrine systems SNS (NEpi) HR, force of contraction PSN (ACh) HR, force of contraction 105 Regulation of Cardiac Output Figure 17.20 Innervation and nervous regulation of the heart. Regulation of Cardiac Output Hormonal regulation - Adrenal medulla – affected by SNS Epi and NEpi - thyroid hormone and glucagon Blood volume – Aldosterone and antidiuretic hormone increase blood vol. incr. C.O. - ANP decreases blood vol. reduces C.O. 107 Regulation of Cardiac Output Other factors that influence cardiac output (Figure 17.21): – [Electrolyte] in ECF – Body temperature SA node fires more rapidly at higher body temp. and more slowly at lower body temp. – Age – Exercise 108 Regulation of Cardiac Output Figure 17.21 Regulation of cardiac output. Heart Failure Heart failure (formerly CHF) = any condition that reduces heart’s ability to pump effectively : myocardial ischemia and/or M.I, valvular heart diseases, any disease of heart muscle (cardiomyopathy) and electrolyte imbalances Heart failure decreased SV reduced C.O. 110 Heart Failure Signs and symptoms of heart failure depend on type of heart failure and side of heart that is affected – LV failure, blood often backs up within pulmonary circuit; known as pulmonary congestion pulmonary edema 111 Heart Failure Both RV and LV failure peripheral edema, in which blood backs up in systemic capillaries (systemic congestion) – Swelling in legs and feet – Peripheral edema exacerbated by kidneys retain excess fluid 112 Heart Failure Treatment – increase cardiac output – Lifestyle modifications -weight loss and mild exercise, dietary sodium and fluid restrictions – Drug therapy – Heart transplant and/or pacemaker 113 Concept Check 1. Name the structures that prevent the AV valves from swinging into the atria during ventricular contraction: Chordae ________________________ tendineae, papillary muscles 2. The valve that separates the LV from the aorta: ______________ Aortic semilunar valve 3. Blood is supplied to the heart muscle by the right and left _______________. coronary arteries 4. Blood from the myocardium is returned to the RA via thecoronary ____________ sinus. 6. Atrial contraction while the ventricles relax, followed by ventricular contraction while the atria relax is cardiac cycle known as _________________. 7. Vagus nerve stimulation on the heart causes (increase/decrease) in HR. 8. A HR of 150 bpm would indicate _____________. tachycardia 9. The stimulus for contraction of the heart is located in the _________________. SA node 10. Heart sounds are due to ___________. valves closing