Human Anatomy & Physiology - Chapter 17 - PDF

Human Anatomy & Physiology Second Edition Chapter 17 The Cardiovascular System I:The Heart PowerPoint® Lectures...

Human Anatomy & Physiology Second Edition Chapter 17 The Cardiovascular System I:The Heart PowerPoint® Lectures created by Suzanne Pundt, University of Texas at Tyler Copyright © 2019, 2016 Pearson Education, Inc. All Rights Reserved OVERVIEW OF THE HEART Copyright © 2019, 2016 Pearson Education, Inc. All Rights Reserved The Cardiovascular System Cardiovascular system: – Consists of heart, blood vessels, and blood – Heart pumps blood (liquid carrying oxygen and nutrients) into blood vessels (system of tubes that distributes it throughout cardiovascular system) Heart—somewhat cone-shaped organ; situated slightly to left side in thoracic cavity; posterior to sternum in mediastinum; rests on diaphragm – Apex—point of cone; points toward left hip; flattened base is posterior side (not inferior) facing posterior rib cage – Relatively small, only about size of fist; generally weighs from 250 to 350 grams (slightly less than 1 pound) Copyright © 2019, 2016 Pearson Education, Inc. All Rights Reserved Location and Basic Structure of the Heart Chambers and external anatomical feature: – Chambers—superior right and left atria (singular, atrium) and inferior right and left ventricles – Externally, indentation known as atrioventricular sulcus is boundary between atria and ventricles – Interventricular sulcus—external depression between right and left ventricles Copyright © 2019, 2016 Pearson Education, Inc. All Rights Reserved 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 arteries (carry blood away from heart) Great vessels—main veins and arteries; bring blood to and from heart Vessels and organs that transport oxygenated blood are color-coded red in textbook; those that carry deoxygenated blood are blue Copyright © 2019, 2016 Pearson Education, Inc. All Rights Reserved Circulation of Blood through the Pulmonary and Systemic Circuits Heart pumps blood through two separate sets of vessels (circuits) Heart is divided functionally into right and left sides Right side of heart is pulmonary pump; pumps blood into series of blood vessels leading to and within lung; collectively called pulmonary circuit Copyright © 2019, 2016 Pearson Education, Inc. All Rights Reserved Circulation of Blood through the Pulmonary and Systemic Circuits – Pulmonary arteries of pulmonary circuit deliver oxygen-poor and carbon dioxide- rich (deoxygenated) blood to lungs – Gas exchange takes place between tiny air sacs in lung (alveoli) and smallest vessels of pulmonary circuit (pulmonary capillaries)  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 deliver this oxygen-rich (oxygenated) blood to left side of heart Copyright © 2019, 2016 Pearson Education, Inc. All Rights Reserved Circulation of Blood through the Pulmonary and Systemic Circuits Left side of heart is systemic pump; receives oxygenated blood from pulmonary veins; pumps it into blood vessels that serve rest of body (systemic circuit) In systemic circuit, arteries deliver oxygenated blood to smallest blood vessels (systemic capillaries) – Here gas exchange occurs again, in reverse:  Oxygen diffuses from blood into tissues  Carbon dioxide diffuses from tissues into blood Copyright © 2019, 2016 Pearson Education, Inc. All Rights Reserved Circulation of Blood through the Pulmonary and Systemic Circuits – Blood delivers nutrients, picks up wastes to be excreted, and distributes hormones to their target cells throughout body – As 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 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 Copyright © 2019, 2016 Pearson Education, Inc. All Rights Reserved Functions of the Heart Heart helps maintain homeostasis of pressure that blood exerts on blood vessels (blood pressure) – Rate and force of heart’s contraction are major factors that influence blood pressure and blood flow to organs – Heart (specifically atria) also acts as endocrine organ; produces atrial natriuretic peptide (ANP)  ANP lowers blood pressure by decreasing sodium ion retention in kidneys  Reduces osmotic water reabsorption and volume and pressure of blood in blood vessels Copyright © 2019, 2016 Pearson Education, Inc. All Rights Reserved The Pericardium, Heart Wall, and Heart Skeleton – Pericardial cavity—between parietal and visceral pericardia; contains very thin layer of serous fluid (pericardial fluid); fluid acts as lubricant, decreasing friction as heart moves – Visceral pericardium rests on top of thin layer of areolar connective tissue; contains large fat deposits (Epicardium) – Myocardium—deep to connective tissue; second and thickest layer of heart wall Copyright © 2019, 2016 Pearson Education, Inc. All Rights Reserved The Pericardium, Heart Wall, and Heart Skeleton Myocardium components: cardiac muscle tissue and fibrous skeleton – Cardiac muscle tissue consists of cardiac muscle cells (myocytes) and their surrounding extracellular matrix – Cardiac muscle cells are attached to and woven through fibrous skeleton; composed of dense irregular collagenous connective tissue; fibrous skeleton functions:  Giving cardiac muscle cells something on which to pull when they contract  Providing structural support  Acting as insulator for heart’s electrical activity Copyright © 2019, 2016 Pearson Education, Inc. All Rights Reserved The Pericardium, Heart Wall, and Heart Skeleton Lumen of heart is lined by endocardium; third and deepest layer of heart wall – Composed of special type of simple squamous epithelium (endothelium) and several layers of connective tissue with elastic and collagen fibers – Endothelial cells of endocardium are continuous with endothelial cells that line blood vessels; share many functions Myocardium Endocardium Epicardium Copyright © 2019, 2016 Pearson Education, Inc. All Rights Reserved The Heart’s Great Vessels, Chambers, and Valves Heart consists of four chambers: two atria and two ventricles: – Atria receive blood from veins, and pump blood into ventricles through valves – Valves have flaps that close when ventricles contract; keep blood from moving backward – Contracting ventricles then eject blood into arteries; carry blood through either systemic or pulmonary circuit Copyright © 2019, 2016 Pearson Education, Inc. All Rights Reserved The Heart’s Great Vessels, Chambers, and Valves Great vessels—bring blood to and away from heart; largest in body: Major systemic veins: two veins that drain majority of systemic circuit are superior and inferior venae cavae; both have large openings into posterior aspect of right atrium: – Superior vena cava (SVC)—drains deoxygenated blood from veins superior to diaphragm – Inferior vena cava (IVC)—drains deoxygenated blood from veins inferior to diaphragm Copyright © 2019, 2016 Pearson Education, Inc. All Rights Reserved The Heart’s Great Vessels, Chambers, and Valves Pulmonary trunk—largest vessel in pulmonary circuit; receives deoxygenated blood pumped from right ventricle – Originates from right ventricle on anterior aspect of heart, nearly along midline – Splits into right and left pulmonary arteries; bring deoxygenated blood to right and left lungs, respectively – Pulmonary arteries branch extensively inside lungs to become tiny pulmonary capillaries where gases are exchanged Copyright © 2019, 2016 Pearson Education, Inc. All Rights Reserved The Heart’s Great Vessels, Chambers, and Valves Oxygenated blood in pulmonary capillaries returns to heart via a set of pulmonary veins – Most people have four; two from each lung – Drain oxygenated blood into posterior part of left atrium Aorta supplies entire systemic circuit with oxygenated blood – Largest and thickest artery in systemic circuit and in entire body – Arises from left ventricle as ascending aorta; curves to left and makes U-turn as aortic arch Copyright © 2019, 2016 Pearson Education, Inc. All Rights Reserved The Heart’s Great Vessels, Chambers, and Valves Figure 17.5a The external anatomy of the heart. Copyright © 2019, 2016 Pearson Education, Inc. All Rights Reserved The Heart’s Great Vessels, Chambers, and Valves Largest structures in heart are four chambers: – Ventricles are larger than atria and have much thicker walls; makes ventricles much stronger pumps – Greater strength is needed to generate pressure that pumps blood around pulmonary and systemic circuits Copyright © 2019, 2016 Pearson Education, Inc. All Rights Reserved The Heart’s Great Vessels, Chambers, and Valves Atria are not symmetrical in size, shape, or location: – Right atrium is larger, thinner-walled, and more anterior than left atrium – Left atrium is thicker-walled, somewhat smaller, and located mostly on posterior side of heart; makes up much of heart’s base (posterior surface) – Fossa ovalis—small indentation in septum; remnant of hole (foramen ovale) in interatrial septum of fetal heart Copyright © 2019, 2016 Pearson Education, Inc. All Rights Reserved The Heart’s Great Vessels, Chambers, and Valves Ventricles—like atria, ventricles are asymmetrical; right ventricle is wider with thinner walls than left ventricle because of pressure differences in pulmonary and systemic circuits – Right ventricle has little resistance against which to pump; left ventricle pumps against much greater resistance – Left ventricle has to work harder than right ventricle; therefore has greater muscle mass; walls are about three times thicker than those of right ventricle; Structure- Function Core Principle Copyright © 2019, 2016 Pearson Education, Inc. All Rights Reserved The Heart’s Great Vessels, Chambers, and Valves Figure 17.6a The internal anatomy of the heart. Copyright © 2019, 2016 Pearson Education, Inc. All Rights Reserved The Heart’s Great Vessels, Chambers, and Valves Blood flow through heart must occur in only one direction so deoxygenated blood goes to pulmonary circuit and oxygenated blood goes to systemic circuit Two types of valves prevent blood from flowing backward No valves needed between atria and veins that drain blood into them Backflow of blood generally doesn’t occur in veins draining into atria – Atria are under very low pressure; blood mostly flows into atria with help of gravity and pressure in veins Copyright © 2019, 2016 Pearson Education, Inc. All Rights Reserved The Heart’s Great Vessels, Chambers, and Valves Forceful ventricular contractions could drive blood backward into atria; prevented by valves between atria and ventricles (right and left atrioventricular (AV) valves) – AV valves consist of flaps (cusps); composed of endocardium overlying core of collagenous connective tissue – Each valve is named for number of cusps:  Tricuspid valve—between right atrium and right ventricle contains three cusps  Bicuspid valve—between left atrium and left ventricle has two cusps; more commonly called mitral valve (clinical name) – Chordae tendineae—fibrous, tendon-like structures attached to inferior end of each cusp  Attached to papillary muscles that contract just before ventricles begin ejecting blood  Creates tension on chordae tendineae keeping valves closed Copyright © 2019, 2016 Pearson Education, Inc. All Rights Reserved The Heart’s Great Vessels, Chambers, and Valves Backflow of blood into ventricles from pulmonary artery and aorta can also occur – Blood flows backward when ventricles relax as result of higher pressure in arteries and gravity; semilunar valves prevent this – “Semilunar” refers to half-moon shape of their three cusps; also composed of endocardium and central collagenous core – Named according to artery in which they reside  Pulmonary valve—between right ventricle and pulmonary trunk  Aortic valve—posterior to pulmonary; between left ventricle and aorta Copyright © 2019, 2016 Pearson Education, Inc. All Rights Reserved The Big Picture of Blood Flow through the Heart Figure 17.8 The Big Picture of Blood Flow through the Heart. Copyright © 2019, 2016 Pearson Education, Inc. All Rights Reserved The Big Picture of Blood Flow through the Heart Figure 17.8 The Big Picture of Blood Flow through the Heart. Copyright © 2019, 2016 Pearson Education, Inc. All Rights Reserved 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 (Figure 17.9) Coronary vessels (coronary arteries): – Ascending aorta—main systemic artery into which left ventricle pumps blood – Immediately after ascending aorta emerges from left ventricle, two branches (right and left coronary arteries) arise; travel in right and left, respectively Copyright © 2019, 2016 Pearson Education, Inc. All Rights Reserved The Coronary Circulation Coronary arterial supply is complicated by formation of anastomoses (systems of channels formed between blood vessels) – Coronary arteries may form anastomoses with one another, with branches from pericardium, or even with arteries from outside coronary circulation entirely – When blood flow to myocardium is insufficient, occasionally new anastomoses will form to provide alternate routes of blood flow (collateral circulation) to myocardium – Collaterals help protect muscle cells from damage that could result from blocked vessels Copyright © 2019, 2016 Pearson Education, Inc. All Rights Reserved The Coronary Circulation Coronary vessels (coronary veins) (Figure 17.9b): – Majority of heart’s veins empty into large venous structure on posterior heart (coronary sinus); drains into posterior right atrium – Coronary sinus receives blood from three major veins:  Great cardiac vein  Small cardiac vein  Middle cardiac vein Copyright © 2019, 2016 Pearson Education, Inc. All Rights Reserved The Coronary Circulation Build-up of fatty material (plaques) in coronary arteries results in coronary artery disease (CAD); leading cause of death worldwide – CAD decreases blood flow to myocardium; results in inadequate oxygenation of myocardium; known as myocardial ischemia – When present, symptoms generally come in form of chest pain (angina pectoris) Copyright © 2019, 2016 Pearson Education, Inc. All Rights Reserved The Coronary Circulation Most dangerous potential consequence of CAD is myocardial infarction (MI; heart attack) – MIs occur when plaques in coronary arteries rupture and clot forms; obstructs blood flow to myocardium; myocardial tissue supplied by that artery infarct (die) – Symptoms include chest pain that radiates along the left arm or left side of neck, shortness of breath, sweating, anxiety, and nausea and/or vomiting – Note: women may not present with chest pain; may suffer back, jaw, or arm pain instead – Survival after MI depends on extent and location of damage  Cardiac muscle cells generally do not undergo mitosis  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 Copyright © 2019, 2016 Pearson Education, Inc. All Rights Reserved The Coronary Circulation – CAD is definitively diagnosed via angiography; small tube is fed through artery in systemic circuit into ascending aorta, and 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 approaches fail, invasive treatments are considered (next slide) Copyright © 2019, 2016 Pearson Education, Inc. All Rights Reserved The Coronary Circulation – Coronary angioplasty—commonly performed invasive procedure; balloon is inflated in blocked artery; piece of wire-mesh tubing (stent) may be inserted into artery to keep it open – Coronary artery bypass grafting—more invasive treatment; other vessels are grafted onto diseased coronary artery to bypass blockage and provide alternate route for blood flow Copyright © 2019, 2016 Pearson Education, Inc. All Rights Reserved Cardiac Muscle Tissue Anatomy and Electrophysiology Copyright © 2019, 2016 Pearson Education, Inc. All Rights Reserved Electrophysiology Heart does not require conscious intervention to elicit cardiac muscle to contract; cardiac muscle exhibits autorhythmicity; sets its own rhythm without need for input from nervous system Cardiac muscle cells contract in response to electrical excitation in form of action potentials Unlike skeletal muscle and many smooth muscle cells, cardiac muscle cells do not require stimulation from nervous system to generate action potentials Cardiac electrical activity is coordinated by very small, unique population of cardiac muscle cells (pacemaker cells) These cells rhythmically and spontaneously generate action potentials; spread to other type of cardiac muscle cell (contractile cells) Copyright © 2019, 2016 Pearson Education, Inc. All Rights Reserved Histology of Cardiac Muscle Tissue and Cells Cardiac muscle cells – Typically branched cells with single nucleus; shorter and wider than skeletal muscle fibers – Contain abundant myoglobin (protein that carries oxygen) – Nearly half of cytoplasmic volume is composed of mitochondria; reflect high energy demands – Possess unique structures (intercalated discs) that join adjacent cardiac muscle cells; join pacemaker cells to contractile cells, and contractile cells to one another – Intercalated discs contain  Desmosomes—hold cardiac muscle cells together  Gap junctions—allow ions to rapidly pass from one cell to another, permitting communication among cardiac muscle cells; Cell-Cell Communication Core Principle Copyright © 2019, 2016 Pearson Education, Inc. All Rights Reserved Electrophysiology of Cardiac Muscle Tissue Pacemaker cells undergo rhythmic, spontaneous depolarizations that lead to action potentials; spread quickly through heart by cardiac conduction system (group of interconnected pacemaker cells) (Figures 17.11–7.12) Action potentials are transmitted from pacemaker cells to contractile cells through intercalated discs that unite them – Gap junctions in these discs allow electrical activity generated by pacemaker cells to rapidly spread to all cardiac muscle cells via electrical synapses – Permits heart to contract as unit and produce coordinated heartbeat; reason cells of heart are sometimes referred to as functional syncytium (term for large, multinucleated cell) Pacemaker cells make up only about 1% of total number of cardiac muscle cells – Three populations of these cells in heart; capable of spontaneously generating action potentials, thereby setting pace of heart – Three cell populations are collectively called cardiac conduction system Copyright © 2019, 2016 Pearson Education, Inc. All Rights Reserved Electrophysiology of Cardiac Muscle Tissue Pacemaker potential—much different from that of contractile cell (Figure 17.11): – Depolarization in pacemaker cell occurs much more slowly; due in part to lack of voltage-gated sodium ion channels in pacemaker sarcolemma – Pacemaker cell action potentials lack plateau phase and membrane potential oscillates—never remains at resting level; instead occurs in cycle, with last event triggering first – Occurs because of nonspecific cation channels; unique to pacemaker cells Copyright © 2019, 2016 Pearson Education, Inc. All Rights Reserved Electrophysiology of Cardiac Muscle Tissue Pacemaker potential (continued) – Slow initial depolarization phase—pacemaker potential starts with plasma membrane in hyperpolarized state—at minimum membrane potential  Opens nonspecific cation channels in membrane; allow sodium ions to leak into cell and potassium ions to leak out  Results in overall slow depolarization to threshold – Full depolarization phase—when membrane reaches threshold, voltage-gated calcium ion channels open; allows calcium ions to enter cell; causes membrane to fully depolarize Copyright © 2019, 2016 Pearson Education, Inc. All Rights Reserved Electrophysiology of Cardiac Muscle Tissue Pacemaker potential (continued) – Repolarization phase—calcium ion channels are time-gated for closing; after certain time (about 100–150 msec), they close; at same time, voltage-gated potassium ion channels begin to open; allows potassium ions to exit cell, and membrane begins to repolarize – Minimum potential phase—potassium ion channels remain open until membrane reaches its minimum potential (membrane is hyperpolarized); opens nonspecific cation channels, and cycle begins again Copyright © 2019, 2016 Pearson Education, Inc. All Rights Reserved Electrophysiology of Cardiac Muscle Tissue Cardiac conduction system includes three populations of pacemaker cells: – Sinoatrial node (SA node)—in upper right atrium, slightly inferior and lateral to opening of superior vena cava  Under normal conditions, SA node has fastest intrinsic rate of depolarization— about 60 or more times per minute  Rate is subject to influence from sympathetic and parasympathetic nervous systems Copyright © 2019, 2016 Pearson Education, Inc. All Rights Reserved Electrophysiology of Cardiac Muscle Tissue Cardiac conduction system cells populations (continued): – Atrioventricular node (AV node)— posterior and medial to tricuspid valve; slower than SA node; intrinsic rate of only about 40 action potentials per minute – Purkinje fiber system—slowest group of pacemaker cells; depolarize only about 20 times per minute; atypical pacemakers because their action potentials rely on different ion channels and they function in slightly different way Copyright © 2019, 2016 Pearson Education, Inc. All Rights Reserved Electrophysiology of Cardiac Muscle Tissue Pacing Heart: Sinus rhythm—each population of pacemaker cells can potentially pace heart (make it beat at certain rate); one that depolarizes fastest sets heart rate; other pacemakers will pace heart only if fastest pacemaker ceases to function – 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 – Note that AV bundle of Purkinje system is only connection between AV node and ventricles  If blocked, SA node cannot pace ventricles even if functioning normally  Purkinje fiber system is capable of pacing heart, but its slow rate of depolarization is not adequate to sustain life beyond short period of time  Occasionally, group of regular contractile cells or pacemaker cells other than SA node will attempt to pace heart at same time as SA node; “extra” pacemaker is called ectopic pacemaker; can cause irregular heart rhythms Copyright © 2019, 2016 Pearson Education, Inc. All Rights Reserved Electrophysiology of Cardiac Muscle Tissue Electrocardiogram (ECG)—important clinical tool for examining health of heart; graphic depiction of electrical activity occurring in all cardiac muscle cells over period of time (Figure 17.14) – Recorded by placing electrodes on surface of patient’s skin: six on chest and two on each extremity – Electrical changes are shown on ECG as deflections (waves); show changes in electrical activity—if there is no net difference, there is no deflection shown – One of most obvious changes in heart revealed by ECG is disturbance in electrical rhythm (dysrhythmia or arrhythmia) Copyright © 2019, 2016 Pearson Education, Inc. All Rights Reserved Electrophysiology of Cardiac Muscle Tissue – ECG recording generally consists of five waves; each represents active depolarization or repolarization of different parts of heart  Small, initial P wave represents depolarization of all cells within atria except SA node; P wave nearly always registers as upward deflection on ECG Copyright © 2019, 2016 Pearson Education, Inc. All Rights Reserved Electrophysiology of Cardiac Muscle Tissue – ECG (continued)  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 upward deflection under normal conditions Copyright © 2019, 2016 Pearson Education, Inc. All Rights Reserved Electrophysiology of Cardiac Muscle Tissue – Periods between waves represent important phases of action potentials and of spread of electrical activity through heart  Intervals include component of at least one wave  Segments do not include any wave components Copyright © 2019, 2016 Pearson Education, Inc. All Rights Reserved Electrophysiology of Cardiac Muscle Tissue – Three intervals of note:  R-R interval—time between two successive R waves; entire duration of generation and spread of action potential through heart; can be measured to determine heart rate  P-R interval—period from beginning of P wave to beginning of R wave; time it takes for depolarization generated by SA node to spread through atria to ventricles; includes AV node delay  Q-T interval—time from beginning of QRS complex to end of T wave; action potentials spread through ventricular cells Copyright © 2019, 2016 Pearson Education, Inc. All Rights Reserved Electrophysiology of Cardiac Muscle Tissue S-T segment—between end of S wave and beginning of T wave – Flat because it is recorded during plateau phase of ventricles; no net changes occur in electrical activity – Elevation or depression of S-T segment is seen with many clinical conditions, most notably myocardial ischemia and myocardial injury and infarction Copyright © 2019, 2016 Pearson Education, Inc. All Rights Reserved Dysrhythmias Cardiac dysrhythmias have three basic patterns: Disturbances in heart rate: – Bradycardia—heart rate under 60 beats per minute – Tachycardia—heart rate over 100 beats per minute; sinus tachycardia is regular, fast rhythm Copyright © 2019, 2016 Pearson Education, Inc. All Rights Reserved Dysrhythmias Disturbances in conduction pathways—normal conduction pathway may be disrupted by accessory pathways between atria and ventricles or by blockage along conduction system (heart block) – Blockage common 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 present; indicates some action potentials from SA node are not being conducted through AV node at all Copyright © 2019, 2016 Pearson Education, Inc. All Rights Reserved Dysrhythmias Disturbances in conduction pathways (continued): – AV node blockage – Another common location for heart blocks is along right or left bundle branch; generally widen QRS complex; depolarization takes longer to spread through ventricles Copyright © 2019, 2016 Pearson Education, Inc. All Rights Reserved Dysrhythmias In fibrillation – Electrical activity in heart essentially goes haywire; causes parts of heart to depolarize and contract while others are repolarizing and not contracting – Fibrillating muscle is often visually compared to writhing movement of plastic bag full of earthworms Copyright © 2019, 2016 Pearson Education, Inc. All Rights Reserved Dysrhythmias Fibrillation (continued): – Atrial fibrillation—generally not life threatening because atrial contraction isn’t necessary for ventricular filling; manifests on ECG tracing as “irregularly irregular” rhythm (no discernible pattern) that lacks P waves Copyright © 2019, 2016 Pearson Education, Inc. All Rights Reserved Dysrhythmias – Ventricular fibrillation—immediately life-threatening and manifests on ECG with chaotic activity  Treated with defibrillation (electric shock to heart); depolarizes all ventricular muscle cells simultaneously and throws cells into their refractory periods  Ideally, SA node will resume pacing heart after shock is delivered Copyright © 2019, 2016 Pearson Education, Inc. All Rights Reserved Dysrhythmias – Ventricular fibrillation is not same as “flat-lining”; condition called asystole  Defibrillation is not used for asystole because heart is not fibrillating; no electrical activity to reset  Treated with CPR and pharmacological agents that stimulate heart such as atropine and epinephrine Copyright © 2019, 2016 Pearson Education, Inc. All Rights Reserved Physiology of the Heart: The Cardiac Cycle Copyright © 2019, 2016 Pearson Education, Inc. All Rights Reserved Introduction to Mechanical Physiology Mechanical physiology—actual processes by which blood fills cardiac chambers and is pumped out of them – Cardiac muscle cells contract as unit to produce one coordinated contraction (heartbeat); muscle cells are arranged in spiral pattern, producing “wringing” action in heart when it contracts – Pressure changes caused by contractions drive blood flow through heart, with valves preventing backflow – Cardiac cycle—sequence of events within heart from one heartbeat to next Copyright © 2019, 2016 Pearson Education, Inc. All Rights Reserved 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 17.15): 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 AV valves are forced shut by blood pushing against them – Both semilunar valves are forced open by outgoing blood Copyright © 2019, 2016 Pearson Education, Inc. All Rights Reserved 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 Copyright © 2019, 2016 Pearson Education, Inc. All Rights Reserved Pressure Changes, Blood Flow, and Valve Function Stethoscope—clinical device that can be used to listen to (auscultate) rhythmic heart sounds: – Under normal conditions, blood flow through open AV and semilunar valves is relatively quiet; sounds occur only when valves close – Sounds are not due to actual valve “slamming shut”; likely result from vibrations of ventricular and blood vessel walls – There are two heart sounds: S1, or “lub,” when AV valves close, and S2, “dub,” when semilunar valves close; S1 is typically longer and louder than S2, although it’s lower in frequency Copyright © 2019, 2016 Pearson Education, Inc. All Rights Reserved Heart Murmurs and Extra Heart Sound One of more common findings on chest auscultation is audible sound called heart murmur; occurs when blood flow through heart is turbulent Heart murmurs are generally caused by defective valves; 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 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 stiff or enlarged ventricle Copyright © 2019, 2016 Pearson Education, Inc. All Rights Reserved Pressure Changes, Blood Flow, and Valve Function Each cardiac cycle consists of one period of relaxation (diastole) and one period of contraction (systole) for each chamber of heart – Atrial and ventricular diastoles and systoles occur at different times as 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; defined by actions of ventricles and positions of valves: filling, contraction, ejection, and relaxation Copyright © 2019, 2016 Pearson Education, Inc. All Rights Reserved Pressure Changes, Blood Flow, and Valve Function Ventricular filling phase of cardiac cycle—period during which blood drains from atria into ventricles – Pressures in left and right ventricles are lower than in atria, pulmonary trunk, and aorta – Higher pressures in pulmonary trunk and aorta cause semilunar valves to be closed; prevents flow of blood from pulmonary trunk and aorta back into ventricles – Atrioventricular valves open because of higher atrial pressure; blood flows down pressure gradient from atria into ventricles – Nearly 80% of total blood volume of atria drains passively in this manner into ventricles – Initially, atria are in diastole, but as blood continues to drain into ventricles, pressure gradient becomes smaller and filling slows Copyright © 2019, 2016 Pearson Education, Inc. All Rights Reserved Pressure Changes, Blood Flow, and Valve Function – At this point, atrial systole takes place and contracting atria eject variable volume of blood into ventricles—as much as remaining 20% of blood volume and as little as few percent – At end of atrial systole, each ventricle contains about 120 ml of blood (end- diastolic volume (EDV)); ventricular volume at end of ventricular diastole Copyright © 2019, 2016 Pearson Education, Inc. All Rights Reserved Pressure Changes, Blood Flow, and Valve Function Beginning of ventricular systole occurs during shortest phase of cardiac cycle (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) Copyright © 2019, 2016 Pearson Education, Inc. All Rights Reserved Pressure Changes, Blood Flow, and Valve Function At beginning of ventricular ejection phase – Pressure in ventricles rises to level higher than in pulmonary trunk and aorta; pushes semilunar valves open; rapid outflow of blood from ventricles occurs – As phase continues, pressure in pulmonary trunk and aorta approaches that in ventricles; at this point, ejection of blood into vessels decreases considerably – Approximately 70 ml of blood pumped from each ventricle; about 50 ml of blood remains in each ventricle (end-systolic volume (ESV)) Copyright © 2019, 2016 Pearson Education, Inc. All Rights Reserved Pressure Changes, Blood Flow, and Valve Function Final phase (isovolumetric relaxation) is brief; occurs as ventricular diastole begins and pressure declines in ventricles – Semilunar valves snap shut; S2 heart sound is heard – Pressure in ventricles is still somewhat higher than in atria; AV valves remain closed – Blood is neither being ejected from nor entering into ventricles; volume briefly remains constant Copyright © 2019, 2016 Pearson Education, Inc. All Rights Reserved Pressure Changes, Blood Flow, and Valve Function Figure 17.17 Events of the cardiac cycle. Copyright © 2019, 2016 Pearson Education, Inc. All Rights Reserved Pressure Changes, Blood Flow, and Valve Function Copyright © 2019, 2016 Pearson Education, Inc. All Rights Reserved Cardiac Output and Regulation Copyright © 2019, 2016 Pearson Education, Inc. All Rights Reserved Introduction to Cardiac Output and Regulation Heart undergoes average of 60–80 cardiac cycles (beats) per minute; 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 (stroke volume (SV)) Copyright © 2019, 2016 Pearson Education, Inc. All Rights Reserved Determination of Cardiac Output Stroke volume (SV) and heart rate (HR) must be known to calculate cardiac output for ventricle: – SV can be calculated by subtracting amount of blood in ventricle at end of contraction (end-systolic volume, or ESV) from amount of blood in ventricle after it has filled during diastole (end-diastolic volume, or EDV) – In average heart, resting stroke volume is equal to about 70 ml: 120 ml (EDV) −50 ml (ESV) = 70 ml (SV) Copyright © 2019, 2016 Pearson Education, Inc. All Rights Reserved Determination of Cardiac Output 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; entire supply of blood passes through heart every minute Copyright © 2019, 2016 Pearson Education, Inc. All Rights Reserved Factors that Influence Stroke Volume Stroke volume averages about 70 ml per beat; may range from 50 to 120 ml; exact stroke volume may be difficult to measure directly; often measurement called ejection fraction is used in its place Ejection fraction—percentage of blood (out of total amount) that is ejected with each ventricular systole; equal to stroke volume divided by EDV; normal ejection fraction is about 50–65%, and this value should be equal for each ventricle Three factors that influence stroke volume: preload, heart contractility, and afterload Copyright © 2019, 2016 Pearson Education, Inc. All Rights Reserved Factors that Influence Stroke Volume – Preload refers to length or degree of stretch of sarcomeres in ventricular cells before they contract; largely determined by EDV (amount of blood that has drained into ventricle by end of filling phase)  Two factors influence EDV: – Length of time ventricle spends in diastole – Amount of blood returning to right ventricle from systemic circuit (venous return)  EDV increases when: – Ventricles spend more time in diastole, because there is more time for them to fill with blood – Left ventricle pumps blood more forcefully into systemic circuit, because additional blood returns to right atrium more rapidly, increasing venous return Copyright © 2019, 2016 Pearson Education, Inc. All Rights Reserved Factors that Influence Stroke Volume – Relationship between preload and stroke volume is explained by mechanism known as Frank-Starling law  According to this law, increased ventricular muscle cells stretch, leads to more forceful contraction  Stretching causes more optimal overlap of actin and myosin filaments in muscle cells; enables stronger contraction and higher stroke volume  Ensures that volume of blood discharged from heart is equal to volume that enters it; particularly important during exercise, when cardiac output must increase to meet body’s needs Copyright © 2019, 2016 Pearson Education, Inc. All Rights Reserved Factors that Influence Stroke Volume – Contractility—heart’s intrinsic pumping ability, or ability to generate tension; difficult to measure directly; can be estimated clinically by examining velocity of blood being ejected from ventricles  Increasing contractility will increase stroke volume and therefore decrease ESV  Decreasing contractility will do opposite: decreasing stroke volume and increasing ESV (assuming that preload and afterload remain constant) Copyright © 2019, 2016 Pearson Education, Inc. All Rights Reserved Factors that Influence Stroke Volume – Contractility (continued):  Agents that affect contractility are known as inotropic agents  Factors that increase heart rate, such as sympathetic nervous stimulation, often also affect contractility and so increase force of contraction  When heart rate is too high, contractility decreases, as does preload; as heart is beating too rapidly to develop significant tension during each contraction decrease in both stroke volume and cardiac output occurs  Stroke volume and heart rate generally increase together Copyright © 2019, 2016 Pearson Education, Inc. All Rights Reserved Factors that Influence Stroke Volume – Afterload refers to force that right and left ventricles must overcome in order to eject blood into their respective arteries  Largely determined by blood pressure in arteries of both pulmonary and systemic circuits  As afterload increases, ventricular pressure must be greater to exceed pressure in arterial pulmonary and systemic vessels and open semilunar valves  Increase in afterload therefore generally causes decrease in stroke volume and rise in ESV of ventricles; conversely, decrease in afterload generally corresponds to higher stroke volume and lower ESV Copyright © 2019, 2016 Pearson Education, Inc. All Rights Reserved 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—make more myofibrils and more organelles, and as result get bigger Copyright © 2019, 2016 Pearson Education, Inc. All Rights Reserved 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 certain point; condition decreases heart lumen and filling space Increases risk for many other cardiac conditions, including heart failure Copyright © 2019, 2016 Pearson Education, Inc. All Rights Reserved 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 (Figure 17.21) Two branches of autonomic nervous system (ANS) regulate our automatic functions Copyright © 2019, 2016 Pearson Education, Inc. All Rights Reserved Regulation of Cardiac Output Role of sympathetic division of ANS includes following: – Innervates heart via set of sympathetic nerves that stem from ganglia located along spinal cord – Neurons release neurotransmitter norepinephrine; increases cardiac output with both positive chronotropic and inotropic effects – Norepinephrine’s positive chronotropic effect increases heart rate by raising rate at which SA node fires, up to 180–200 or more times per minute; increases entry of calcium ions into cardiac muscle cells – Higher calcium ion concentration increases contractility of cardiac muscle cells; in turn raises stroke volume; together, these two effects can dramatically increase heart rate Copyright © 2019, 2016 Pearson Education, Inc. All Rights Reserved Regulation of Cardiac Output Parasympathetic nervous system exerts essentially opposite effects on heart; innervates heart by left and right vagus nerves (CN X) – Release acetylcholine; primarily affects SA node, decreasing rate of action potential generation – Slows heart rate and can even stop heart temporarily if parasympathetic stimulation is strong enough – Vagus nerves primarily innervate atrial muscle; have less effect on ventricular contractility than on heart rate; therefore have only weak negative inotropic effects Copyright © 2019, 2016 Pearson Education, Inc. All Rights Reserved 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— positive inotropic and chronotropic agents—but effect is longer-lasting than sympathetic stimulation – Other hormones that also have positive inotropic and chronotropic effects include thyroid hormone and glucagon produced by pancreas Copyright © 2019, 2016 Pearson Education, Inc. All Rights Reserved Regulation of Cardiac Output – Amount of water in blood (blood volume) plays significant role in determining heart’s preload and therefore its strength of contraction  Hormones such as 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 Copyright © 2019, 2016 Pearson Education, Inc. All Rights Reserved Regulation of Cardiac Output Other factors that influence cardiac output (Figure 17.22): – Concentration of certain electrolytes in extracellular fluid plays large role in determining length and magnitude of 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 Copyright © 2019, 2016 Pearson Education, Inc. All Rights Reserved Regulation of Cardiac Output Other factors that influence cardiac output (continued): – Age and physical fitness influence heart rate and cardiac output; younger children and elderly often have higher resting heart rate; trained athletes often have much lower resting heart rate – Exercise increases stroke volume, so for body to maintain constant cardiac output, heart rate must decrease Copyright © 2019, 2016 Pearson Education, Inc. All Rights Reserved Heart Failure Heart failure—as any condition that reduces heart’s ability to function effectively as 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 Copyright © 2019, 2016 Pearson Education, Inc. All Rights Reserved Heart Failure Signs and symptoms of heart failure generally depend on type of heart failure and side of heart that is affected – In left ventricular failure, blood often backs up within pulmonary circuit; known as pulmonary congestion – Backup of blood flow increases pressure in these vessels, driving fluid out of pulmonary capillaries and into lungs; called pulmonary edema Copyright © 2019, 2016 Pearson Education, Inc. All Rights Reserved Heart Failure Both right and left ventricular failure may produce 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; often causes visible swelling, especially in legs and feet, where fluid collects as 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 lower cardiac output) Copyright © 2019, 2016 Pearson Education, Inc. All Rights Reserved 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, heart transplant and/or surgically implanted pacemaker that electrically stimulates and paces heart may be necessary Copyright © 2019, 2016 Pearson Education, Inc. All Rights Reserved