Amerman Chapter 17: Cardiovascular System I: The Heart PDF

ERIN C. AMERMAN FLORIDA STATE COLLEGE AT JACKSONVILLE Lecture Presentation by Suzanne Pundt University of Texas at Tyler © 2016 Pearson Education, Inc.  LEARNING OBJECTIVES 1. Basic Anatomy and Function of the Cardiovascular System - I...

ERIN C. AMERMAN FLORIDA STATE COLLEGE AT JACKSONVILLE Lecture Presentation by Suzanne Pundt University of Texas at Tyler © 2016 Pearson Education, Inc.  LEARNING OBJECTIVES 1. Basic Anatomy and Function of the Cardiovascular System - Identify and describe the anatomical structures of the heart, including chambers, valves, and major blood vessels. - Explain the functional roles of these structures in the mechanics of blood circulation. 2. Electrophysiology of the Heart - Understand the conduction system of the heart, including the sinoatrial node, atrioventricular node, and Purkinje fibers. - Interpret normal electrocardiograms 3. Cardiac Cycle Dynamics - Describe the phases of the cardiac cycle, including ventricular filling, systole, diastole, and the associated pressure and volume changes. - Analyze the impact of these phases on blood flow through the heart, using graphical interpretations of pressure and volume changes. © 2016 Pearson Education, Inc.  LEARNING OBJECTIVES CONTINUED 4. Cardiovascular Responses to Physiological Stress - Assess how the cardiovascular system adjusts to acute and chronic physiological changes such as exercise, hypertension, and altitude. - Explore the compensatory mechanisms and their limits in maintaining homeostasis during stress conditions. 5. Pathophysiology of Cardiac Diseases - Understand the pathophysiological mechanisms leading to common cardiovascular diseases such as coronary artery disease, valvular heart diseases, and heart failure. - Discuss clinical findings, including symptoms, diagnostic test results, and potential treatments, with the underlying pathophysiological processes. 6. Ethical and Social Implications - Reflect on the ethical, social, and economic factors influencing cardiovascular treatment choices, healthcare access, and patient outcomes. - Engage in discussions about the impact of lifestyle, socioeconomic status, and global health disparities on cardiovascular disease prevalence and management. © 2016 Pearson Education, Inc.  THE CARDIOVASCULAR SYSTEM Cardiovascular system – consists of heart, blood vessels, and blood; heart pumps blood (liquid carrying oxygen and nutrients) into blood vessels, a system of tubes that distributes it throughout cardiovascular system © 2016 Pearson Education, Inc.  LOCATION AND BASIC STRUCTURE OF THE HEART Heart – somewhat cone-shaped organ, situated slightly to left side in thoracic Cardiomegaly cavity, posterior to sternum in mediastinum; rests on diaphragm  Apex – point of cone; points toward left hip; its flattened base is its posterior side (not inferior) facing posterior rib cage  Relatively small organ, only about size of fist; generally weighs from 250 to 350 grams (What if it’s bigger than Image from Radiopaedia.org that?) © 2016 Pearson Education, Inc.  LOCATION AND BASIC STRUCTURE OF THE HEART Figure 17.1a Location and basic anatomy of the heart in the thoracic cavity. © 2016 Pearson Education, Inc.  LOCATION AND BASIC STRUCTURE OF THE HEART Chambers and external anatomical features  Chambers – superior right and left atria (singular, atrium) and inferior right and left ventricles  Externally, an indentation known as atrioventricular sulcus is found at boundary between the atria and ventricles  Interventricular sulcus – external depression located between right and left ventricles © 2016 Pearson Education, Inc. LOCATION AND BASIC STRUCTURE OF THE HEART Both right and left atria receive blood from veins, (blood vessels that bring blood to heart) Blood drains from atria to ventricles; ventricles pump blood into blood vessels called arteries (carry blood away from heart) Main veins and arteries that bring blood to and from heart are known as great vessels © 2016 Pearson Education, Inc.  CIRCULATION OF BLOOD THROUGH THE PULMONARY AND SYSTEMIC CIRCUITS Heart pumps blood through two separate sets of vessels, or circuits Heart is divided functionally into right and left sides Right side of heart is pulmonary pump because it pumps blood into a series of blood vessels leading to and within lungs; collectively called pulmonary circuit  Pulmonary arteries of pulmonary circuit deliver oxygen-poor and carbon dioxide-rich, or deoxygenated, blood to lungs © 2016 Pearson Education, Inc. CIRCULATION OF BLOOD THROUGH THE PULMONARY AND SYSTEMIC CIRCUITS  Gas exchange takes place between tiny air sacs in lung (alveoli) and smallest vessels of pulmonary circuit (pulmonary capillaries)  During gas exchange, oxygen diffuses from air in alveoli into blood in pulmonary capillaries; carbon dioxide diffuses from blood in pulmonary capillaries to air in alveoli, to be expired  Veins of pulmonary circuit then deliver this oxygen-rich (oxygenated) blood to left side of heart  Vessels and organs that transport oxygenated blood are color-coded red in textbook; those that carry deoxygenated blood are blue © 2016 Pearson Education, Inc. CIRCULATION OF BLOOD THROUGH THE PULMONARY AND SYSTEMIC CIRCUITS Left side of heart is systemic pump; receives oxygenated blood from pulmonary veins and pumps it into blood vessels that serve rest of body (collectively called systemic circuit)  In systemic circuit, arteries deliver oxygenated blood to smallest blood vessels (systemic capillaries)  Here gas exchange occurs again, except in reverse: Oxygen diffuses from blood into tissues, and carbon dioxide diffuses from tissues into blood © 2016 Pearson Education, Inc.  CIRCULATION OF BLOOD THROUGH THE PULMONARY AND SYSTEMIC CIRCUITS  Blood also delivers nutrients, picks up wastes to be excreted, and distributes hormones to their target cells throughout body  As a result of gas exchange in tissues, blood is deoxygenated and veins of systemic circuit then deliver it back to right side of heart, to be pumped into pulmonary circuit Pulmonary circuit is a low-pressure circuit because it pumps blood only to lungs; systemic circuit is a high- pressure circuit because it has to pump blood to entire rest of body © 2016 Pearson Education, Inc. WHEN PEOPLE SAY HYPERTENSION, WHAT DO THEY MEAN? Pulmonary vs. Systemic HTN Birnso O et al. © 2016 Pearson Education, Inc.  THE PERICARDIUM, HEART WALL, AND HEART SKELETON Pericardium – membranous structure surrounding heart; composed of following structures Fibrous pericardium – tough outer layer, Low distensibility helps to prevent chambers of heart from overfilling with blood Serous pericardium – thin inner serous membrane that produces serous fluid:1. Parietal pericardium – fused to inner surface of fibrous pericardium; encases heart like a sac, but when it reaches great vessels, it folds under itself and forms another layer that adheres directly to heart; 2. Visceral pericardium – innermost layer; also known as epicardium; considered most superficial layer of heart wall Pericardial cavity – found between parietal and visceral pericardia; contains a very thin layer of serous fluid (pericardial fluid); acts as a lubricant, decreasing friction as heart moves © 2016 Pearson Education, Inc.  THE PERICARDIUM, HEART WALL, AND HEART SKELETON Myocardium - Cardiac muscle tissue consists of cardiac muscle cells Layers of the heart wall (myocytes) and their surrounding extracellular matrix Lumen of heart is lined by endocardium; third and deepest layer of heart wall  Endocardium is composed of a special type of simple squamous epithelium called endothelium  Endothelial cells of endocardium are continuous with endothelial cells that line blood vessels © 2016 Pearson Education, Inc.  CARDIAC TAMPONADE If pericardial cavity becomes filled with excess fluid, cardiac tamponade may result; many potential causes, including trauma, recent thoracic surgery, and pericarditis. Regardless of cause, result is same – because fibrous pericardium is strong but not very flexible, excess fluid in pericardial cavity squeezes heart; reduces capacity of ventricles to fill with blood, compromising amount of blood pumped with each beat Treatment may include a procedure in which excess fluid is removed via a needle inserted into the pericardial cavity © 2016 Pearson Education, Inc.  THE CORONARY CIRCULATION Heart’s chambers are filled with blood, but myocardium is too thick for oxygen and nutrients to diffuse from inside chambers to all of organ’s cells. For this reason, heart is supplied by a set of blood vessels collectively called coronary circulation Consists of coronary arteries and veins © 2016 Pearson Education, Inc.  THE CORONARY CIRCULATION First two branches of the aorta : right and left coronary arteries, which travel in right and left atrioventricular sulci, respectively  Right coronary artery branches - Largest branch is marginal artery, then continues as the posterior interventricular artery (posterior descending artery, PDA, different from Patent Ductus Arteriosus)  Left coronary artery branches - Anterior interventricular artery (left anterior descending artery, or LAD) and Circumflex artery (LCX) © 2016 Pearson Education, Inc.  THE CORONARY CIRCULATION Coronary veins:  Generally, majority of heart’s veins empty into a large venous structure on posterior heart, called coronary sinus; drains into posterior right atrium  Coronary sinus receives blood from three major veins: o Great cardiac vein o Small cardiac vein o Middle cardiac vein © 2016 Pearson Education, Inc.  THE CORONARY CIRCULATION A buildup of fatty material called plaques in coronary arteries results in coronary artery disease, or CAD; leading cause of death worldwide  CAD decreases blood flow to myocardium; results in inadequate oxygenation of myocardium, a condition known as myocardial ischemia  When present, symptoms generally come in form of chest pain; referred to as angina pectoris © 2016 Pearson Education, Inc.  THE CORONARY CIRCULATION Most dangerous potential consequence of CAD is a myocardial infarction (MI), or heart attack  An MI occurs when plaques in coronary arteries rupture and a clot forms that obstructs blood flow to myocardium; myocardial tissue supplied by that artery infarct, or die  Symptoms of an MI include chest pain that radiates along dermatomes to left arm or left side of neck, shortness of breath, sweating, anxiety, and nausea and/or vomiting  Note that women may not present with chest pain and may suffer back, jaw, or arm pain instead © 2016 Pearson Education, Inc.  THE CORONARY CIRCULATION  Survival after an MI depends on extent and location of damage; cardiac muscle cells generally do not undergo mitosis, and so after an MI, dead cells are replaced with fibrous, noncontractile scar tissue  Death of part of myocardium increases workload of remaining heart muscle  Risk factors for CAD and MI include smoking, high blood pressure, poorly controlled diabetes, high levels of certain lipids in blood, obesity, age over 40 for males and over 50 for females, genetics, and male gender © 2016 Pearson Education, Inc. THE CORONARY CIRCULATION  CAD is definitively diagnosed via angiography; a small tube is fed through an artery in systemic circuit into ascending aorta, and finally into coronary arteries; special dye is injected into arteries, and their condition is examined by x-ray  Treatments include lifestyle modifications and appropriate medications; if these two approaches fail, then invasive treatments are considered © 2016 Pearson Education, Inc.  THE CORONARY CIRCULATION  A commonly performed invasive procedure is coronary angioplasty, during which a balloon is inflated in blocked artery and a piece of wire-mesh tubing called a stent may be inserted into artery to keep it open  A more invasive treatment is coronary artery bypass grafting, during which other vessels are grafted onto diseased coronary artery to bypass blockage and provide an alternate route for blood flow © 2016 Pearson Education, Inc.  EXTERNAL HEART ACTIVITY Have completed before coming to class. © 2016 Pearson Education, Inc.  THE HEART’S GREAT VESSELS, CHAMBERS, AND VALVES Figure 17.5a The external anatomy of the heart. © 2016 Pearson Education, Inc.  THE HEART’S GREAT VESSELS, CHAMBERS, AND VALVES Figure 17.5c The external anatomy of the heart. © 2016 Pearson Education, Inc.  THE HEART’S GREAT VESSELS, CHAMBERS, AND VALVES Heart consists of four chambers: two atria and two ventricles (Figures 17.5–17.7):  Atria receive blood from veins, and pump blood into ventricles through structures called valves  Valves have flaps that close when ventricles contract, keeping blood from moving backward  Contracting ventricles then eject blood into arteries; carry blood through either systemic or pulmonary circuit © 2016 Pearson Education, Inc.  THE HEART’S GREAT VESSELS, CHAMBERS, AND VALVES Atria are not symmetrical in size, shape, or location:  Externally, each atrium has a muscular pouch called an auricle; named for their resemblance to external ear; expand to give atria more space in which to hold blood  Interatrial septum – thin wall that separates two atria  Fossa ovalis – small indentation in septum; remnant of a hole known as foramen ovale present in interatrial septum of fetal heart © 2016 Pearson Education, Inc.  THE HEART’S GREAT VESSELS, CHAMBERS, AND VALVES Ventricles – ventricles are asymmetrical; right ventricle is wider and has thinner walls than left ventricle because of pressure differences in pulmonary and systemic circuits  Each ventricle also contains finger-like projections of muscle (papillary muscles); attach by tendon-like cords called chordae tendineae to valves located between atria and ventricles  A thick, muscular wall, interventricular septum, separates right and left ventricles; © 2016 Pearson Education, Inc.  ATRIAL SEPTAL DEFECT AND VENTRICULAR SEPTAL DEFECT The American Heart Association, heart.org © 2016 Pearson Education, Inc. INTERNAL HEART ACTIVITY © 2016 Pearson Education, Inc.  THE HEART’S GREAT VESSELS, CHAMBERS, AND VALVES Figure 17.6 The internal anatomy of the heart, anterior dissection. © 2016 Pearson Education, Inc.  THE HEART’S GREAT VESSELS, CHAMBERS, AND VALVES Backflow of blood from ventricles into atria could occur because their forceful contractions could drive blood backward into atria  Backward flow is prevented by valves between atria and ventricles, called right and left atrioventricular (or AV) valves  AV valves consist of flaps, called cusps; named for number of cusps it contains: tricuspid valve between right atrium and right ventricle and bicuspid valve (mitral valve) between left atrium and left ventricle © 2016 Pearson Education, Inc.  THE HEART’S GREAT VESSELS, CHAMBERS, AND VALVES Blood is stopped from flowing back into ventricles by two valves called semilunar valves  Backflow of blood can also become a problem in pulmonary artery and aorta, because blood begins to flow backward when ventricles relax as a result of higher pressure in arteries and gravity  “Semilunar” refers to half-moon shape of their three cusps; also composed of endocardium and a central collagenous core  Named according to artery in which they reside; pulmonary valve is located between right ventricle and pulmonary trunk; aortic valve is posterior to it between left ventricle and aorta © 2016 Pearson Education, Inc.  VALVULAR HEART DISEASES Valvular heart diseases impair function of one or more of valves; may be congenital (present at birth) or acquired from a disease process such as infection, cancer, or disorders of immune system Two major types of valvular defects: insufficiency and stenosis  Insufficient valve – fails to close fully and so allows blood to leak backward  Stenotic valve – calcium deposits have built up in cusps, making them hard and inflexible; blood flows through a stenotic valve with difficulty; often heart has to pump harder to eject blood through it Both types of valvular heart diseases may cause an audible “swooshing” of blood when heart beats, called a heart murmur Other signs and symptoms vary with type and severity of disease but may include enlargement of heart, fatigue, dizziness, and heart palpitations Mitral and aortic valves are most commonly affected by valvular heart disease © 2016 Pearson Education, Inc.  GROUP DISCUSSION 1. What would happen if someone has aortic stenosis? 2. What about mitral stenosis? 3. What about pulmonic stenosis and tricuspid stenosis? 4. What about aortic and mitral regurgitation? © 2016 Pearson Education, Inc. HEART MODEL ACTIVITY © 2016 Pearson Education, Inc. FLOW OF BLOOD THROUGH THE HEART ACTIVITY © 2016 Pearson Education, Inc.  Use the following 20 steps below for guidance! Low Oxygen, Gas Exchange, Oxygenated RIGHT ATRIUM R. A.V. VALVE (TRICUSPID) 20 RIGHT VENTRICLE PULMONARY SEMILUNAR VALVE STEP PULMONARY TRUNK R. AND L. PULMONARY ARTERIES R. AND L. LUNGS (GAS EXCHANGE) S R. AND L. PULMONARY VEINS LEFT ATRIUM L. A. V. VALVE (MITRAL OR BICUSPID) LEFT VENTRICLE AORTIC SEMILUNAR VALVE AORTA SYSTEMIC ARTERIES ARTERIOLES CAPILLARIES (GAS EXCHANGE) VENULES SYSTEMIC VEINS SUPERIOR AND INFERIOR VENA CAVA AND CORONARY SINUS RIGHT ATRIUM © 2016 Pearson Education, Inc. HISTOLOGY OF CARDIAC MUSCLE TISSUE AND CELLS  Cardiac muscle cells contain abundant myoglobin (protein that carries oxygen) and mitochondria; reflect their high energy demands  Possess unique structures called intercalated discs that join adjacent cardiac muscle cells, and gap junctions that allow ions to rapidly pass from one cell to another, permitting communication among cardiac muscle cells.  Permits heart to contract as a unit and produce a coordinated heartbeat; sometimes referred to as a functional syncytium (sin- shish-e-um) © 2016 Pearson Education, Inc.  ELECTROPHYSIOLOGY Heart does not require conscious input for cardiac muscle to contract; cardiac muscle exhibits autorhythmicity, meaning it sets its own rhythm without a need for input from nervous system Cardiac electrical activity is coordinated by a very small, unique population of cardiac muscle cells called pacemaker cells Pacemaker cells undergo rhythmic, spontaneous depolarizations that lead to action potentials; spread quickly through heart by cardiac conduction system © 2016 Pearson Education, Inc.  ELECTROPHYSIOLOGY Sequence of events of a contractile cell action potential resembles that of a skeletal muscle fiber action potential with one important exception: plateau phase  If cardiac action potentials lasted only about 1–5 msec, like skeletal muscle fiber action potentials, resting heart rate would be about 15 times faster than it should be at rest  Plateau phase lengthens cardiac action potential to about 200–300 msec; slows heart rate, providing time required for heart to fill with blood preventing tetany(sustained contraction) © 2016 Pearson Education, Inc.  ELECTROPHYSIOLOGY  Sarcoplasmic reticulum of cardiac muscle cells is much less extensive than in skeletal muscle fibers; does not release enough calcium ions to produce a reliably strong contraction  Remaining calcium ions needed for contraction diffuse into cell through calcium ion channels  For this reason, concentration of calcium ions in cardiac extracellular fluid plays a significant role in determining strength of contraction, illustrating one reason why calcium ion homeostasis is so critical © 2016 Pearson Education, Inc.  ELECTROPHYSIOLOGY Cardiac conduction system  Sinoatrial node (SA node) – located in upper right atrium, SA node has fastest intrinsic rate of depolarization—about 60 or more times per minute  Atrioventricular node (AV node) – located posterior and medial to tricuspid valve  Purkinje fiber system - Atrioventricular bundle (AV bundle) inferior interatrial septum and superior interventricular septum  Right and left bundle branches course along right and left sides of interventricular septum,  Terminal branches penetrate ventricles and finally come into contact with contractile cardiac muscle cells © 2016 Pearson Education, Inc.  ELECTROPHYSIOLOGY  SA node is normal pacemaker of entire heart; electrical rhythms generated and maintained by SA node are known as sinus rhythms  AV node and Purkinje fiber system normally only conduct action potentials generated by SA node; if SA node ceases to function, AV node can successfully pace heart, albeit somewhat slowly © 2016 Pearson Education, Inc.  ELECTROPHYSIOLOGY Electrocardiogram (ECG) – important clinical tool for examining health of heart; graphic depiction of electrical activity occurring in all cardiac muscle cells over a period of time Small, initial P wave represents depolarization of all cells within atria except SA node; P wave nearly always registers as an upward deflection on ECG. Large QRS complex represents ventricular depolarization; actually three separate waves; Q wave is first downward deflection; R is large upward deflection; S is following downward deflection. Small T wave occurs after S wave of QRS complex; represents ventricular repolarization; T wave is an upward deflection under normal conditions Periods between waves represent important phases of action potentials and of spread of electrical activity through heart. Intervals include a component of at least one wave, Segments do not include any wave components © 2016 Pearson Education, Inc.  ELECTROPHYSIOLOGY Figure 17.13 A normal electrocardiogram (ECG) tracing. © 2016 Pearson Education, Inc.  ELECTROPHYSIOLOGY Figure 17.13 A normal electrocardiogram (ECG) tracing. © 2016 Pearson Education, Inc.  DYSRHYTHMIAS Cardiac dysrhythmias have three basic patterns: Disturbances in heart rate:  Bradycardia – is a heart rate under 60 beats per minute  Tachycardia – is a heart rate over 100 beats per minute; sinus tachycardia is a regular, fast rhythm © 2016 Pearson Education, Inc.  DYSRHYTHMIAS Disturbances in conduction pathways – normal conduction pathway may be disrupted by accessory pathways between atria and ventricles or by a blockage along conduction system, called a heart block  Often found at AV node; P-R interval is longer than normal, due to increased time for impulses to spread to ventricles through AV node; extra P waves are present, which indicates that some action potentials from SA node are not being conducted through AV node at all © 2016 Pearson Education, Inc.  DYSRHYTHMIAS In fibrillation, electrical activity in heart essentially goes haywire, causing parts of heart to depolarize and contract while others are repolarizing and not contracting  Fibrillating muscle is often visually compared to writhing movement of a plastic bag full of earthworms © 2016 Pearson Education, Inc.  MECHANICAL PHYSIOLOGY Mechanical physiology refers to actual processes by which blood fills cardiac chambers and is pumped out of them  Cardiac muscle cells contract as a unit to produce one coordinated contraction, called a heartbeat; muscle cells are arranged in a spiral pattern, producing a “wringing” action in heart when it contracts  Pressure changes caused by contractions drive blood flow through heart, with valves preventing backflow; sequence of events that take place within heart from one heartbeat to the next is known as cardiac cycle © 2016 Pearson Education, Inc.  PRESSURE CHANGES, BLOOD FLOW, AND VALVE FUNCTION When ventricles contract, their pressures rise above those in right and left atria and in pulmonary trunk and aorta; causes blood to flow from ventricles to vessels and produces two changes in valves:  Both of AV valves are forced shut by blood pushing against them  Both of semilunar valves are forced open by outgoing blood © 2016 Pearson Education, Inc.  PRESSURE CHANGES, BLOOD FLOW, AND VALVE FUNCTION When ventricles relax, opposite occurs; pressures in ventricles fall below those in atria and in pulmonary trunk and aorta  Higher pressure in atria 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 © 2016 Pearson Education, Inc.  PRESSURE CHANGES, BLOOD FLOW, AND VALVE FUNCTION Stethoscope – clinical device that can be used to listen to (auscultate) rhythmic heart sounds (Figure 17.15):  Under normal conditions, blood flow through open AV and semilunar valves is relatively quiet; sounds occur only when valves close  There are two heart sounds: S1, or “lub,” is heard when AV valves close, and S2, “dub,” is heard when semilunar valves close © 2016 Pearson Education, Inc.  HEART MURMURS AND EXTRA HEART SOUNDS One of the more common findings on chest auscultation is an audible sound called a heart murmur; occurs when blood flow through heart is turbulent Heart murmurs are generally caused by defective valves, although they may also result from defective chordae tendineae or holes in interatrial or interventricular septum Children, however, often have heart murmurs that do not represent defects © 2016 Pearson Education, Inc.  HEART MURMURS AND EXTRA HEART SOUNDS Chest auscultation may also reveal extra heart sounds  S3 – can occur just as blood begins to flow into ventricles, right after S2; results from recoil of ventricular walls as they are stretched and filled  S4 – heard when most of blood has finished draining from atria to ventricles, just before S1; typically results from blood being forced into a stiff or enlarged ventricle  Both S3 and S4 may represent pathology, but they can also occasionally be heard in a healthy heart © 2016 Pearson Education, Inc.  PRESSURE CHANGES, BLOOD FLOW, AND VALVE FUNCTION Each cardiac cycle consists of one period of relaxation called diastole and one period of contraction called systole for each chamber of heart  Atrial and ventricular diastoles and systoles occur at different times as a result of AV node delay; both sides of heart are working to pump blood into their respective circuits simultaneously  Cycle is divided into four main phases that are defined by actions of ventricles and positions of valves: filling, contraction, ejection, and relaxation © 2016 Pearson Education, Inc.  CARDIAC CYCLE Ventricular filling phase of cardiac cycle is period during which blood drains from atria into ventricles  Higher pressures in pulmonary trunk and aorta cause semilunar valves to be closed; Atrioventricular valves open because of higher atrial pressure  Nearly 80% of total blood volume of atria drains passively in this manner into ventricles  At this point, atrial systole takes place and contracting atria eject a variable volume of blood into ventricles  At end of atrial systole, each ventricle contains about 120 ml of blood; volume known as end-diastolic volume (EDV) because it is ventricular volume at the end of ventricular diastole © 2016 Pearson Education, Inc.  CARDIAC CYCLE Beginning of ventricular systole occurs during shortest phase of cardiac cycle, called isovolumetric contraction  Pressure in ventricles rises rapidly as ventricles begin to contract; high pressure closes AV valves and causes S1 heart sound  Ventricular pressure is not yet high enough to push open semilunar valves, so both sets of valves are closed and ventricular volume does not change (same volume = isovolumetric) © 2016 Pearson Education, Inc.  CARDIAC CYCLE At beginning of ventricular ejection phase, pressure in ventricles rises to a level higher than that in pulmonary trunk and aorta; pushes semilunar valves open;  Ventricular ejection phase sees approximately 70 ml of blood pumped from each ventricle; means that about 50 ml of blood remains in each ventricle, a volume known as end-systolic volume (ESV) © 2016 Pearson Education, Inc.  CARDIAC CYCLE Final phase, called isovolumetric relaxation, is brief; occurs as ventricular diastole begins and pressure declines in ventricles  Semilunar valves snap shut, at which point S2 heart sound is heard  Pressure in ventricles is still somewhat higher than that in atria, so AV valves remain closed  Blood is neither being ejected from nor entering into ventricles and their volume briefly remains constant © 2016 Pearson Education, Inc.  CARDIAC OUTPUT AND REGULATION Heart undergoes an average of 60–80 cardiac cycles or beats per minute, a value known as heart rate (HR)  HR is one determinant of cardiac output (CO), amount of blood pumped into pulmonary and systemic circuits in 1 minute  CO is also determined by amount of blood pumped in one heartbeat, called stroke volume (SV)  SV can be calculated by subtracting amount of blood in ventricle at end of a contraction (end-systolic volume, or ESV) from amount of blood in ventricle after it has filled during diastole (end-diastolic volume, or EDV)  In an average heart, resting stroke volume is equal to about 70 ml:  120 ml (EDV) – 50 ml (ESV) = 70 ml (SV) © 2016 Pearson Education, Inc.  CARDIAC OUTPUT AND REGULATION To find cardiac output, multiply heart rate by stroke volume:  72 beats/min (HR) × 70 ml/beat (SV) = 5040 ml/min, or ~5 liters/min (CO)  Resting cardiac output averages about 5 liters/min; right ventricle pumps about 5 liters into pulmonary circuit and left ventricle pumps same amount into systemic circuit in 1 minute  Normal adult blood volume is about 5 liters, so entire supply of blood passes through heart every minute © 2016 Pearson Education, Inc.  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. © 2016 Pearson Education, Inc.  HOW CHANGES IN PRELOAD, CONTRACTILITY, AND AFTERLOAD AFFECT STROKE VOLUME © 2016 Pearson Education, Inc.  HOW CHANGES IN PRELOAD, CONTRACTILITY, AND AFTERLOAD AFFECT STROKE VOLUME © 2016 Pearson Education, Inc.  VENTRICULAR HYPERTROPHY 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 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 © 2016 Pearson Education, Inc. REGULATION OF CARDIAC OUTPUT Although heart is autorhythmic, it still requires regulation to ensure that cardiac output meets body’s needs at all times Regulated primarily by nervous and endocrine systems, which influence both heart rate and stroke volume Two branches of autonomic nervous system (ANS) regulate our automatic functions Innervates heart via a set of sympathetic nerves that stem from ganglia located along spinal cord Neurons release neurotransmitter norepinephrine; increases cardiac output Parasympathetic nervous system exerts essentially opposite effects on heart; innervates heart by left and right vagus nerves (CN X). These nerves release acetylcholine; primarily affects SA node, decreasing its rate of action potential generation. Vagus nerves primarily innervate atrial muscle, so they have less effect on ventricular contractility than on heart rate © 2016 Pearson Education, Inc.  REGULATION OF CARDIAC OUTPUT Figure 17.20 Innervation and nervous regulation of the heart. © 2016 Pearson Education, Inc. REGULATION OF CARDIAC OUTPUT Hormonal regulation of cardiac output occurs in various forms  Adrenal medulla is activated by sympathetic nervous system, and in response it secretes hormones epinephrine and norepinephrine into bloodstream  Hormones have same effects as sympathetic nervous system neurotransmitters— but effect is longer-lasting than sympathetic stimulation Amount of water in blood (blood volume) plays a significant role in determining heart’s preload and therefore its strength of contraction  aldosterone and antidiuretic hormone increase blood volume and preload, and so raise cardiac output  Atrial natriuretic peptide, decreases blood volume and preload, and therefore reduces cardiac output © 2016 Pearson Education, Inc. REGULATION OF CARDIAC OUTPUT Other factors that influence cardiac output (Figure 17.21):  Concentration of certain electrolytes in extracellular fluid plays a large role in determining length and magnitude of an action potential and cardiac output  Body temperature influences CO; SA node fires more rapidly at higher body temperatures and more slowly at lower body temperatures  Age and physical fitness influence heart rate and cardiac output; younger children and elderly often have a higher resting heart rate, whereas trained athletes often have a much lower resting heart rate  Exercise increases stroke volume, so for body to maintain a constant cardiac output, heart rate must decrease © 2016 Pearson Education, Inc.  HEART FAILURE Heart failure is defined as any condition that reduces heart’s ability to function effectively as a pump: Causes of heart failure include reduced contractility due to myocardial ischemia and/or myocardial infarction, valvular heart diseases, any disease of heart muscle itself (known as cardiomyopathy), and electrolyte imbalances Heart failure generally results in decreased stroke volume, which in turn reduces cardiac output © 2016 Pearson Education, Inc.  HEART FAILURE Signs and symptoms of heart failure generally depend on type of heart failure and side of heart that is affected 1. In left ventricular failure, blood often backs up within pulmonary circuit; known as pulmonary congestion. This backup of blood flow increases pressure in these vessels, driving fluid out of pulmonary capillaries and into lungs, a condition called pulmonary edema 2. Both right and left ventricular failure may produce a similar finding in systemic circuit: peripheral edema, in which blood backs up in systemic capillaries (systemic congestion). This backup forces fluid out of capillaries and into tissues, which often causes visible swelling, especially in legs and feet, where fluid collects as a result of gravity. Peripheral edema is exacerbated by fact that kidneys retain excess fluid during heart failure (in order to increase preload and compensate for a lower cardiac output) © 2016 Pearson Education, Inc.  HEART FAILURE Treatment – generally aimed at increasing cardiac output  Lifestyle modifications may include weight loss and mild exercise plus dietary sodium and fluid restrictions  Drug therapy increases cardiac output in one of at least three ways: decreasing abnormally high preload by promoting fluid loss from kidneys, increasing heart’s contractility so that it pumps more effectively, and decreasing afterload so that ventricles have to pump against lower pressure  In some cases, a heart transplant and/or a surgically implanted pacemaker that electrically stimulates and paces heart may be necessary © 2016 Pearson Education, Inc.  TESTING-FOUNDATION 1. What is the function of the atrioventricular valves in the heart? A) To pump blood into the arteries B) To prevent backflow of blood into the atria when the ventricles contract C) To carry oxygenated blood to the tissues D) To remove carbon dioxide from the blood 2. What is the primary function of the heart's semilunar valves? A) They regulate blood flow from the atria to the ventricles. B) They prevent backflow of blood from the arteries into the ventricles. C) They control the flow of blood between the heart and the lungs. D) They facilitate the exchange of gases in the blood. 3. Which chamber of the heart receives oxygen-depleted blood from the systemic circulation? A) Right atrium B) Left atrium C) Right ventricle D) Left ventricle © 2016 Pearson Education, © 2016 Pearson I Education, Inc.  TESTING-FOUNDATION 4. Where does the exchange of gases occur within the cardiovascular system? A) In the heart ventricles B) In the coronary arteries C) In the capillaries of the lungs and tissues D) In the atria of the heart 5. Which of the following vessels carries oxygen-rich blood back to the heart? A) Pulmonary artery B) Aorta C) Pulmonary vein D) Coronary artery 6. What is the role of the papillary muscles? A) They contract to open the heart valves. B) They prevent the atrioventricular valves from inverting. C) They direct the flow of blood through the heart. D) They absorb excess calcium from the bloodstream. © 2016 Pearson Education, © 2016 Pearson I Education, Inc. TESTING-PATHOPHYSIOLOGY 1. What is a common pathophysiological effect of chronic hypertension on the heart? A) Reduction in ventricular filling B) Decreased myocardial contractility C) Left ventricular hypertrophy D) Decreased stroke volume 2. In aortic stenosis, the left ventricle has to work harder because: A) It faces increased afterload due to narrowed aortic valve. B) There is a backflow of blood from the aorta. C) It compensates for reduced preload. D) The mitral valve also typically shows signs of stenosis. 3. Mitral valve prolapse can lead to mitral regurgitation (blood backflow), which causes: A) Increased preload in the left atrium. B) Decreased end-diastolic volume in the left ventricle. C) Increased afterload in the left ventricle. D) Decreased cardiac output due to effective forward flow. © 2016 Pearson Education, © 2016 Pearson I Education, Inc.  Longitudinal Case Study: The Journey of a Troubled Heart: John Davis' Story ~45 min; Recommend finishing case studies from chapters 22 and 23 first; Additional Systems Involved: Nervous, GI, Endocrine/Nutrition. Patient Profile: Name: John Davis Age: 65 years old Sex: Male Occupation: Retired civil engineer Initial Presentation: John presents with increasing shortness of breath, fatigue, and occasional chest pain over the past six months. © 2016 Pearson Education, © 2016 Pearson I Education, Inc.  Learning Objectives: (Submit a short essay focusing on whatever you think are important in less than 300 words) 1. Foundational Anatomy and Physiology - Identify the anatomical structures and functions of the heart. - Understand the physiological mechanisms of blood flow and cardiac output. 2. Pathophysiological Impacts - Describe the effects of hypertension on the heart. - Describe the effects of hyperlipidemia on cardiovascular health. - Describe the effects of aortic stenosis on heart function. - Explain heart failure pathophysiology and describe its symptoms. 3. Multi-System Involvement - Discuss the role of the vagus nerve in heart rate regulation. - Discuss the impact of diabetes on cardiovascular and GI physiology (Endocrine chapter). © 2016 Pearson Education, © 2016 Pearson I Education, Inc.  Detailed History: At age 40, John was diagnosed with hypertension (BP: 150/90 mmHg) and started on Lisinopril (10 mg daily). His blood pressure control was inconsistent due to poor lifestyle habits. At age 45, he was diagnosed with hyperlipidemia (total cholesterol: 250 mg/dL, LDL: 160 mg/dL, HDL: 35 mg/dL, triglycerides: 200 mg/dL) and prescribed atorvastatin (20 mg daily). He struggled with dietary changes. By age 50, John developed type 2 diabetes (fasting glucose: 140 mg/dL, HbA1c: 7.5%). He was prescribed metformin (500 mg twice daily) but had variable blood glucose control. At age 60, John suffered an MI in the LAD artery. He had severe chest pain radiating to his left arm, with troponin I at 10 ng/mL and EKG showing ST elevation in leads V1-V4. He underwent angioplasty with stent placement and was prescribed aspirin (81 mg daily) and clopidogrel (75 mg daily). © 2016 Pearson Education, © 2016 Pearson I Education, Inc.  Detailed History Continued: At age 63, he was diagnosed with aortic stenosis after experiencing dizziness and shortness of breath. He was advised regular monitoring and potential valve replacement. Now, at 65, John is on a regimen including lisinopril, atorvastatin, metformin, aspirin, clopidogrel, carvedilol (25 mg twice daily), and nitroglycerin PRN. His most recent lab values (Recall lab indications from previous case studies; will NOT be on your BIO202 tests so relax) show moderate control: BP 145/85 mmHg, fasting glucose 130 mg/dL, HbA1c 7.2%, total cholesterol 220 mg/dL, LDL 140 mg/dL, HDL 38 mg/dL, triglycerides 180 mg/dL, creatinine 1.1 mg/dL, eGFR 85 mL/min/1.73m², troponin I 0.03 ng/mL, BNP 150 pg/mL. He struggles with heart failure symptoms and diabetic gastroparesis (delayed gastric emptying). © 2016 Pearson Education, © 2016 Pearson I Education, Inc.  Group Discussion: 1. Foundational Anatomy and Function of the Heart Question: What are the major anatomical structures of the heart, and how do their functions facilitate effective cardiac output and systemic circulation? Hint: Consider the roles of the atria and ventricles in pumping blood, as well as how valves regulate blood flow direction. Use lab manual and textbook diagram if needed. 2. Physiological Mechanisms of Blood Flow and Cardiac Output: Question: How do variations in heart rate and stroke volume impact cardiac output, and what physiological mechanisms regulate these changes? Hint: Think about how sympathetic and parasympathetic nervous systems alter heart rate. © 2016 Pearson Education, © 2016 Pearson I Education, Inc.  Group Discussion: 3. Impact of Hypertension on Cardiac Function Question: How does prolonged hypertension affect the structural and functional integrity of the heart, specifically in terms of left ventricular hypertrophy and its long-term consequences? Hint: Focus on the concept of afterload and its effects on cardiac muscle workload and eventual cardiac remodeling. 4. Hyperlipidemia's Role in Cardiovascular Health Question: Discuss how hyperlipidemia contributes to the development of atherosclerosis and the potential for acute coronary events. Hint: Recall the role of LDL discussed in Chapter 23 and how plaque stability can be compromised. © 2016 Pearson Education, © 2016 Pearson I Education, Inc.  Group Discussion: 5. Consequences of Aortic Stenosis on Heart Function: Question: In what ways does aortic stenosis compromise cardiac output, and how does this condition interact with the pathophysiology of other cardiovascular diseases discussed? Hint: Focus on the concept of ventricular pressure overload and how it leads to hypertrophy. 6. Heart failure is a complex pathophysiological process. What conditions do you think contributed to John’s heart failure? Hint: Everything…but let’s count. © 2016 Pearson Education, © 2016 Pearson I Education, Inc.