* Your assessment is very important for improving the workof artificial intelligence, which forms the content of this project
Download Ch.-20-Lecture-wo
Cardiac contractility modulation wikipedia , lookup
Heart failure wikipedia , lookup
Antihypertensive drug wikipedia , lookup
Management of acute coronary syndrome wikipedia , lookup
Hypertrophic cardiomyopathy wikipedia , lookup
Artificial heart valve wikipedia , lookup
Electrocardiography wikipedia , lookup
Coronary artery disease wikipedia , lookup
Mitral insufficiency wikipedia , lookup
Lutembacher's syndrome wikipedia , lookup
Cardiac surgery wikipedia , lookup
Myocardial infarction wikipedia , lookup
Arrhythmogenic right ventricular dysplasia wikipedia , lookup
Quantium Medical Cardiac Output wikipedia , lookup
Heart arrhythmia wikipedia , lookup
Dextro-Transposition of the great arteries wikipedia , lookup
Chapter 20: The Heart Primary sources for figures and content: Marieb, E. N. Human Anatomy & Physiology. 6th ed. San Francisco: Pearson Benjamin Cummings, 2004. Martini, F. H. Fundamentals of Anatomy & Physiology. 6th ed. San Francisco: Pearson Benjamin Cummings, 2004. The cardiovascular system and heart. The Cardiovascular System Figure 20–1 The Cardiovascular System • Pulmonary circuit: – Carries blood to and from gas exchange surfaces of lungs – Right ventricle  lungs  left atrium • Systemic circuit: – Carries blood to and from the body – Left ventricle  body  right atrium 3 Types of Blood Vessels • Arteries: – carry blood away from heart • Veins: – carry blood to heart • Capillaries (exchange vessels): – networks between arteries and veins – Exchange materials between blood and tissues – Dissolved gases, nutrients, wastes The heart and its general features. Anatomy of the Heart • Located directly behind sternum Figure 20–2a The Heart • Location: – Left of midline, between 2nd rib and 5th intercostal space – posterior to sternum, in pericardial cavity in mediastinum • Heart is fist sized, < 1 lb • Beats 100,000 times/day moving 8,000 Liters blood/day • Surrounded by pericardium: – serous and fibrous layers • Serous membranes: visceral and parietal – secrete pericardial fluid, reduce friction The Heart 1. Pericarditis – Inflammation of pericardium, usually due to infection – Causes friction 2. Cardiac tamponade – Buildup of fluid in pericardial space – Restricts heart movement Internal Anatomy Figure 20–6a 4 Chambers of the Heart • 2 for each circuit: – left and right: 2 ventricles and 2 atria 2 Atria – – – – Superior, thin walls Smooth posterior walls internally Pectinate muscles (ridges) anteriorly has expandable flap called an auricle lateral and superior – Left and right separated by interatrial septum 4 Chambers of the Heart 2 Ventricles – Inferior, thick walls, lined with trabeculae carneae (muscular ridges) – Left and right separated by interventricular septum – Left ventricle 3x thicker, 5x more friction while pumping, same volume as right • WHY? – Left is round, right is crescent Left and Right Ventricles • Have significant structural differences Figure 20–7 The Left Ventricle • Systemic circulation: – blood leaves left ventricle through aortic valve into ascending aorta – ascending aorta  aortic arch 4 Chambers of the Heart • Right atrium: – collects blood from systemic circuit • Right ventricle: – pumps blood to pulmonary circuit • Left atrium: – collects blood from pulmonary circuit • Left ventricle: – pumps blood to systemic circuit Relation to Thoracic Cavity Figure 20–2b The Heart: External Divisions • Great veins and arteries at the base • Pointed tip is apex Figure 20–2c 2 Layers of Pericardium 1. Parietal pericardium: – outer layer 2. Visceral pericardium: – inner layer of pericardium Superficial Anatomy of the Heart Figure 20–3 Sulci • Coronary sulcus: – divides atria and ventricles • Anterior and posterior interventricular sulci: – separate left and right ventricles – contain blood vessels of cardiac muscle The layers of the heart wall. The Heart Wall Figure 20–4 3 Layers of the Heart Wall 1. Epicardium (thin): outer layer – Visceral pericardium: serous membrane • Loose CT attached to myocardium 2. Myocardium (thick): middle layer – Cardiac muscle tissue with CT, vessels, and nerves 3. Endocardium (thin): inner layer – Simple squamous epithelium lining with basal lamina – Continuous with endothelium blood vessesl Cardiac Muscle Cells Figure 20–5 Cardiac Muscle Tissue • Muscle cells = cardiocytes • Uses actin and myosin sliding filaments to contract • Rich in mitochondria, resists fatigue but dependent on aerobic respiration • Cells connected by intercalated discs • Contraction is all or none • Longer contractile phase than skeletal muscle • Fibrous skeleton of the heart (tough CT) acts as the tendon Cardiac Muscle Cells • Intercalated discs: – – – – – interconnect cardiac muscle cells secured by desmosomes linked by gap junctions convey force of contraction propagate action potentials The path of blood flow through the heart, and the major blood vessels, chambers, and heart valves. Internal Anatomy Figure 20–6a The Vena Cava • Delivers systemic circulation to right atrium • Superior vena cava: – receives blood from head, neck, upper limbs, and chest • Inferior vena cava: – receives blood from trunk, and viscera, lower limbs The Heart Valves • One-way valves prevent backflow during contraction Figure 20–8 Atrioventricular (AV) Valves • Connect atria to ventricles • Permit blood flow in 1 direction: – atria to ventricles • Flaps = cusps • Pressure closes valve cusps during ventricular contraction 1. Tricuspid valve: right side, 3 cusps 2. Bicuspid/Mitral valve: left side, 2 cusps Cusps • Cusps attached to chordae tendineae from papillary muscles on ventricle wall • Contraction of papillary muscles prevent cusps opening backward during ventricle contraction – Prevent back flow • Cusps hang loose when ventricles not contraction, allow ventricles to fill with blood Semilunar Valves • • • • Between ventricles and arteries 3 cusps No chordae tendineae or muscles Forced open by blood from ventricular contraction • Snap closed to prevent backflow Heart Disorders 1. Valvular heart disease - Valve function deteriorates to extent that heart cannot maintain adequate circulation - Rheumatic fever: childhood reaction to streptococcal infection, chronic carditis, VHD in adult 2. Heart murmur - Leaky valve - Mitral valve prolapse: murmur of left AV valve, cusps don’t close properly, blood regurgitates back into left atrium Heart Disorders 3. Congestive heart failure – Decreased pumping efficiency • Diseased valves, damaged muscle – Blood backs up  fluid leaks from vessels and collects in lungs and tissues Blood Flow Through the Heart The Pulmonary Circuit • Pulmonary trunk divides into left and right pulmonary arteries • Blood flows from right ventricle to pulmonary trunk through pulmonary semilunar valve Return from Pulmonary Circuit • Blood from the lungs gathers into left and right pulmonary veins • Pulmonary veins deliver to left atrium • Blood from left atrium passes to left ventricle through left atrioventricular (AV) valve (bicuspid valve or mitral valve) Damage to the semilunar valve on the right side of the heart would affect blood flow to which vessel? A. B. C. D. aorta superior vena cava pulmonary artery coronary artery What prevents the AV valves from opening back into the atria? A. B. C. D. papillary muscles valve cusps moderator band chordae tendineae Why is the left ventricle more muscular than the right ventricle? A. Because it must pump a larger volume. B. Because it must generate more force. C. Because it must open a tighter atrioventricular valve. D. Both A and B are correct. Fetal Heart: Adapted to bypass lungs Foramen Ovale • Before birth, is an opening through interatrial septum in the right atrium • Connects the 2 atria • ~25% of blood bypasses directly the left atrium • Closes at birth leaving scar called fossa ovalis Ductus arteriosus • Connects pulmonary trunk to aorta • ~90% of blood bypasses lungs • Closes at birth leaving the ligamentum arteriosum Failure of either to close = poor oxygenation of blood, cyanosis, “blue baby syndrome” KEY CONCEPT • The heart has 4 chambers: – 2 for pulmonary circuit: • right atrium and right ventricle – 2 for systemic circuit: • left atrium and left ventricle • Left ventricle has a greater workload – more massive than right ventricle, but the two chambers pump equal amounts of blood • AV valves prevent backflow from ventricles into atria • Semilunar valves prevent backflow from aortic and pulmonary trunks into ventricles Blood supply to the heart. Blood Supply to the Heart • Coronary circulation Figure 20–9 Coronary Circulation • • • • • Coronary arteries and cardiac veins Supplies blood to muscle tissue of heart Heart = <1% body mass, requires 5% of blood Too thick for diffusion Coronary arteries – originate at base of ascending aorta – branch to capillary beds for diffusion • Blood returns via cardiac veins – Cardiac veins empty into right atrium Right Coronary Artery • Supplies blood to: – right atrium – portions of both ventricles – cells of sinoatrial (SA) and atrioventricular nodes – marginal arteries • surface of right ventricle Left Coronary Artery • Supplies blood to: – left ventricle – left atrium – interventricular septum Coronary artery disease • Partial or complete block of coronary circulation, results in coronary ischemia • Can lead to myocardial infraction (heart attack) – Heart tissue denied oxygen dies • Common symptom – Angina pectoralis: • plan in the chest, especially during activity, as a result of ischemia Coronary bypass surgery • Use healthy veins (from legs) to create anatomoses around blockages • Most people have 4 major coronary arteries  “quadruple bypass” The Cardiac Cycle Figure 20–11 The Heartbeat • A single contraction of the heart • 1% myocardial cells autorhythmic – Depolarize without neural or endocrine stimulation • Depolarization transmitted to other myocardial cells through cardiac conduction system 1. Sinoatrial (SA) node 2. Atrioventricular (AV) node 3. Conducting cells Structures of the Conducting System 1. SA node: – Right atrium wall near superior vena cava 2. AV node: – Inferior portion of interatrial septum above tricuspid valve Structures of the Conducting System 3. Conducting cells: – controls and coordinates heartbeat – In the atrium: • Interconnect SA and AV nodes – Connect nodes and myocardium – Distribute stimulus through myocardium • Run down interventricular septum and around apex – In the ventricles: AV bundle, bundle branches and Purkinji fibers The Cardiac Cycle • Begins with action potential at SA node – gradually depolarizes toward threshold – transmitted through conducting system – produces action potentials in cardiac muscle cells (contractile cells) • SA node Also called pacemaker potential • SA node depolarizes first, establishing heart rate • Cells of nodes cannot maintain resting membrane potential, drift to depolarization: – SA node: 80-100 action potentials/min • “natural pacemaker” – AV node: 40-60 action potentials/min • Resting rate (sinus rhythm) – ~75 bpm set by SA node + parasympathetic stimulation Figure 20–12 The Conducting System Figure 20–12 The components and functions of the conducting system of the heart. Impulse Conduction through the Heart Figure 20–13 The Sinoatrial (SA) Node • In posterior wall of right atrium • Contains pacemaker cells • Connected to AV node by internodal pathways • Begins atrial activation (Step 1) The Atrioventricular (AV) Node • • • • In floor of right atrium Receives impulse from SA node (Step 2) Delays impulse (Step 3) Atrial contraction begins The AV Bundle • In the septum • Carries impulse to left and right bundle branches: – which conduct to Purkinje fibers (Step 4) • And to the moderator band: – which conducts to papillary muscles 4. The Purkinje Fibers • Distribute impulse through ventricles (Step 5) • Atrial contraction is completed • Ventricular contraction begins Total time = ~370 ms Abnormal Pacemaker Function • Normal average heart rate = ~70-80 bpm – Max = ~230 bpm, but inefficient above 180 1. Bradycardia: <60 bpm – abnormally slow heart rate 2. Tachycardia: >100 bpm – abnormally fast heart rate If the cells of the SA node failed to function, how would the heart rate be affected? A. B. C. D. It It It It would would would would be faster. be slower. be irregular. not change. In a person with bradycardia, is cardiac output likely to be greater than or less than normal? A. greater than normal B. less than normal Why is it important for impulses from the atria to be delayed at the AV node before they pass into the ventricles? A. to prevent backflow of atrial blood B. to allow complete ventricular contraction C. to allow complete atrial emptying D. to create more forceful ventricular contraction The electrical events that are associated with a normal electrocardiogram (EKG). The Electrocardiogram Figure 20–14b Electrocardiogram (ECG or EKG) • A recording of electrical events in the heart • Obtained by electrodes at specific body locations • Abnormal patterns diagnose damage Features of an ECG • P wave: atria depolarize – Depolarization wave from SA node through atria ~80ms • QRS complex: ventricles depolarize – Atrial repolarization and ventricle depolarization ~80ms • T wave: – Ventricle repolarization ~160ms Time Intervals & Diagnosis of Heart Problems • P–R interval: – from start of atrial depolarization, to start of QRS complex – P-R longer than 200 ms = damage to AV node or conducting cells • Total heart block = – Cause = damage AV node, – Effect = no impulses transmitted through, atria and ventricles beat independently (atria fast, ventricles slow) Time Intervals & Diagnosis of Heart Problems • Q–T interval: – from ventricular depolarization, to ventricular repolarization – Longer than 380 ms = coronary ischemia or myocardial damage EKG used to diagnose heart problems 1. Cardiac Arrhythmias – Abnormal patterns of cardiac electrical activity 2. Fibrillation – Rapid, irregular, out of phase contractions due to activity in areas other than SA node – Defibrillation to stop all activity so SA node can resume control KEY CONCEPT • Heart rate is normally established by cells of SA node • Rate can be modified by autonomic activity, hormones, and other factors • From the SA node, stimulus is conducted to AV node, AV bundle, bundle branches, and Purkinje fibers before reaching ventricular muscle cells • Electrical events associated with the heartbeat can be monitored in an electrocardiogram (ECG) The events that take place during an action potential in cardiac muscle. Contractile Cells • Purkinje fibers distribute the stimulus to the contractile cells, which make up most of the muscle cells in the heart Action Potentials in Skeletal and Cardiac Muscle Figure 20–15 The events that take place during the cardiac cycle, including atrial and ventricular systole and diastole. The Cardiac Cycle • The period between the start of 1 heartbeat and the beginning of the next • Alternation contraction and relaxation 2 Phases of the Cardiac Cycle • Within any 1 chamber: – systole (contraction) • Contraction • High pressure • Blood gets pushed to next chamber – diastole (relaxation) • Relaxation • Low pressure • Chamber fills with blood Blood Flow • Blood flows from high to low pressure: – controlled by timing of contractions – directed by one-way valves Phases of the Cardiac Cycle Figure 20–16 4 Phases of the Cardiac Cycle 1. 2. 3. 4. Atrial systole Atrial diastole Ventricular systole Ventricular diastole Cardiac Cycle and Heart Rate • At 75 beats per minute: – cardiac cycle lasts about 800 msecs • When heart rate increases: – all phases of cardiac cycle shorten, particularly diastole Cardiac Cycle: Pressure and Volume Figure 20–17 8 Steps in the Cardiac Cycle 1. Atrial systole begins: – – atrial contraction begins right and left AV valves are open 2. Atria eject blood into ventricles: – filling ventricles 3. Atrial systole ends: – – AV valves close ventricles contain maximum volume 8 Steps in the Cardiac Cycle 4. Ventricular systole: 1st phase – – – ventricular contraction pressure in ventricles rises AV valves shut 5. Ventricular systole (ejection): 2nd phase – – – Pressure in ventricle rises and exceeds pressure in the arteries semilunar valves open blood flows into pulmonary and aortic trunks 8 Steps in the Cardiac Cycle 6. Ventricular pressure falls: – semilunar valves close 7. Ventricular diastole: – – At start ventricular pressure is higher than atrial pressure and all heart valves are closed Then ventricles relax 8 Steps in the Cardiac Cycle 8. Ventricular diastole: Atrial pressure is higher than ventricular pressure – – AV valves open Blood fills the relaxed atria • – Atria contraction only adds ~30% more to ventricles (can live with bad atria) cardiac cycle ends Incr. heart rate  decr. cycle time, decr. diastole time  decr. time to fill Heart sounds relate to specific events in the cardiac cycle. Heart Sounds Figure 20–18b Heart Sounds • S1: “lubb” – produced by AV valves closing at start of ventricular systole • S2: “dubb” – produced by semilunar valves closing at start of ventricular diastole • S3, S4: – soft sounds – blood flow into ventricles and atrial contraction Cardiac output and the factors that influence it. Cardiodynamics • The movement and force generated by cardiac contractions • CO = cardiac output – Amount of blood pumped by each ventricle in one minute, depends on heart rate and stroke volume – CO = HR x SV Important Cardiodynamics Terms • End-diastolic volume (EDV) ~ 120 ml – Volume of blood in ventricle before contraction • End-systolic volume (ESV) ~ 50 ml – Volume of blood in ventricle following a beat – Typically 50 ml • Stroke volume (SV): ~ 70 ml – Amount of blood pumped by ventricle SV = EDV — ESV Usually SV is constant, you need to change HR to increase CO as needed. Stroke Volume • Volume (ml) of blood ejected per beat Figure 20–19 Cardiac Output • Cardiac output (CO) ml/min = • Heart rate (HR) beats/min  • Stroke volume (SV) ml/beat Heart rate effectors. Overview: Control of Cardiac Output Figure 20–20 (Navigator) HR affected by: 1. Autonomic nervous input – Parasympathetic stimulation • slows the heart – Sympathetic stimulation • speeds the heart 2. Hormones 3. Venous return – More blood return = incr. HR – Stretch receptors in right atrium • trigger incr. heart rate through incr. sympathetic activity 4. Other factors: ions, drugs Cardiac Output • At 160-180 bpm CO is at max: – Incr. HR  decr. time to fill ventricles – If ventricle is not full  decr. SV and CO • Conditioning can incr. SV and decr. HR • Fit athletes can – incr. max CO by 700% – decr. resting HR by 50% with same CO due to incr. SV Variables that influence stroke volume and heart rate effectors. Heart Rate Effectors 1. Autonomic Innervations – SA node, AV node and atrial myocardium innervated by both sympathetic (NE) and parasympathetic (Ach) nerve fibers equally – Sympathetic dominated in ventricles – Cardiac centers in medulla oblongata monitor blood pressure and gasses to adjust HR • A) Cardioacceleratory center – sympathetic • B) Cardioinhibitory center parasympathetic Heart Rate Effectors 1. Autonomic Innervations – Parasympathetic tone reduce rate of SA node • 72-80 bpm females • 64-72 bpm males • 40 bpm athletes 2. Hormones – Epinephrine, Norepinephrine, thyroxine all increase HR by acting at SA node – Beta blockers: treats hypertension • Blocks B-receptors for E/NE thus preventing sympathetic stimulation Other Heart Rate Effectors • Caffeine – Rapid depolarization of SA node, incr. HR • Nicotine – Stimulates sympathetic neurons, incr. HR • Hyperkalemia – High K+, inhibits repolarization – Beats week, heart can stop Other Heart Rate Effectors • Hypercalcemia – High Ca+ – Muscle cells excitable, incr. HR – Can cause prolonged contraction  heart seizes • Hypocalcemia – Low Ca+ – Contractions weak  heart can stop • Temperature – Affects metabolic rate of cardiocytes – High temp  incr. HR – Low temp  decr. HR What effect does drinking large amounts of caffeinated drinks have on the heart? A. B. C. D. increased heart rate decreased heart rate erratic heart rate bradycardia If the cardioinhibitory center of the medulla oblongata were damaged, which part of the autonomic nervous system would be affected, and how would the heart be influenced? A. parasympathetic; increased heart rate B. parasympathetic; decreased heart rate C. sympathetic; increased heart rate D. sympathetic; decreased heart rate Factors Affecting Stroke Volume Figure 20–23 (Navigator) Factors Affecting Heart Rate and Stroke Volume Figure 20–24 KEY CONCEPT • Cardiac output: – the amount of blood pumped by the left ventricle each minute – adjusted by the ANS in response to: • circulating hormones • changes in blood volume • alterations in venous return What effect would stimulating the acetylcholine receptors of the heart have on cardiac output? A. It would output. B. It would output. C. It would output. D. It would increase cardiac decrease cardiac cause erratic cardiac have no effect. What effect would an increase in venous return have on the stroke volume? A. It would increase stroke volume. B. It would decrease stroke volume. C. It would cause erratic stroke volume. D. It would have no effect. Joe’s end-systolic volume is 40 ml, and his end-diastolic volume is 125 ml. What is Joe’s stroke volume? A. B. C. D. 165 ml 155 ml 85 ml 100 ml SUMMARY • Organization of cardiovascular system: – pulmonary and systemic circuits • 3 types of blood vessels: – arteries, veins, and capillaries • 4 chambers of the heart: – left and right atria – left and right ventricles • Pericardium, mediastinum, and pericardial sac • Coronary sulcus and superficial anatomy of the heart • Structures and cells of the heart wall SUMMARY • Internal anatomy and structures of the heart: – septa, muscles, and blood vessels • Valves of the heart and direction of blood flow • Connective tissues of the heart • Coronary blood supply • Contractile cells and the conducting system: – pacemaker calls, nodes, bundles, and Purkinje fibers SUMMARY • Electrocardiogram and its wave forms • Refractory period of cardiac cells • Cardiac cycle: – atrial and ventricular – systole and diastole • Cardiodynamics: – stroke volume and cardiac output • Control of cardiac output