Slide 1

THE CARDIOVASCULAR SYSTEM: THE HEART Slide 2 HEART LOCATION Size, Location, and Orientation: The heart is the size of a fist and weighs 250-300 grams The heart is found in mediastinum and two-thirds lies left of the midsternal line The base is directed toward the right shoulder and the apex points toward the left hip Slide 3 HEART LOCATION Slide 4 Coverings of the Heart The heart is enclosed in a double-walled sac called the pericardium: The loosely fitting superficial part of this sac is the fibrous pericardium (tough, dense connective tissue) Protects the heart Anchors it to surrounding structures Prevents overfilling of the heart with blood Deep to fibrous pericardium is the serous pericardium: Thin, slippery, two-layer serous membrane The parietal pericardium lines the internal surface of the fibrous pericardium Then parietal pericardium turns inferiorly and continues over the external heart surface as the visceral pericardium, or epicardium, which is an integral part of the heart wall Between the parietal and visceral layers is the slitlike pericardial cavity, which contains a film of serous fluid The serous membranes, lubricated by the fluid, glide smoothly past one another during heart activity, allowing the mobile heart to work in a relatively friction-free environment Slide 5 Coverings of the Heart Slide 6 HOMEOSTATIC IMBALANCE Pericarditis: inflammation of the pericardium Hinders production of serous fluid and roughens the serous membrane surface Heart rubs against its pericardial sac creating a creaking noise (pericardial friction rub) that can be heard with a stethoscope Deep pain to the sternum Pericardia stick together and impede heart activity Severe cases: Large amounts of inflammatory fluid seeps into the pericardial cavity compressing the heart, limiting its ability to pump blood (cardiac tamponade) Treated by inserting a syringe into the pericardial cavity and draining off the excess fluid Slide 7 Layers of the Heart The heart wall is composed of three layers, all richly supplied with blood vessels Superficial epicardium is the visceral layer of the serous pericardium Often infiltrated with fat, especially in older people Middle layer, myocardium,is composed mainly of cardiac muscle and forms the bulk of the heart It is the layer that contracts Cardiac muscle cells are tethered to one another by crisscrossing connective tissue fibers and arranged in spiral or circular bundles reinforcing the myocardium internally and anchors the cardiac muscle fibers The third layer, the endocardium (squamous epithelium), lines the chambers of the heart and is continuous with the endothelial linings of the blood vessels leaving and entering the heart Slide 8 HEART LAYERS Slide 9 CARDIAC MUSCLE Slide 10 CHAMBERS and ASSOCIATED GREAT VESSELS Heart has four chambers: Two superior atria Two inferior ventricles Internal partition that divides the heart longitudinally is called the interatrial septum where it separates the atria, and the interventricular septum where it separates the ventricles Right ventricle forms most of the anterior surface of the heart Left ventricle dominates the infero-posterior aspect of the heart and forms the heart apex Slide 11 CHAMBERS and ASSOCIATED GREAT VESSELS Two grooves visible on the heart surface indicate the boundaries of its four chambers and carry the blood vessels supplying the myocardium The atrioventricular groove, or coronary sulcus, encircles the junction of the atria and ventricles like a crown Slide 12 CHAMBERS and ASSOCIATED GREAT VESSELS The anterior interventricular sulcus, cradling the anterior interventricular artery, marks the anterior position of the septum separating the right and left ventricles It continues as the posterior interventricular sulcus, which provides a similar landmark on the hearts posteroinferior surface Slide 13 CHAMBERS and ASSOCIATED GREAT VESSELS Slide 14 Slide 15 HEART ANATOMY Slide 16 Atria: The Receiving Chambers Small, wrinkled, protruding appendages called auricles increase the atrial volume Internally: Posterior portion smooth- walled Anterior portion the walls are ridged with bundles of muscle tissue (pectinate muscles) Anterior and posterior regions are separated by a ridge called the crista terminalis Interatrial septum bears a shallow depression (fossa ovalis), that marks the spot where an opening, the foramen ovale, existed in the fetal heart Slide 17 INTERNAL HEART ANATOMY Slide 18 Atria: The Receiving Chambers Slide 19 Receiving chambers for blood returning to the heart from the circulation Small, thin-walled chambers which contract only minimally to push blood next door into the ventricles Blood enters the right atrium via three veins: Superior vena cava returns blood from body regions superior to the diaphragm Inferior vena cava returns blood from body areas below the diaphragm Coronary sinus collects blood draining from myocardium Blood enters the left atrium via four veins: Pulmonary veins transport blood from the lungs back to the heart Slide 20 Atria: The Receiving Chambers Slide 21 Ventricles: The Discharging Chambers Together the ventricles make up most of the volume of the heart Marking the internal walls of the ventricular chambers are irregular ridges of muscle called trabeculae carneae which add support and strength Papillary muscles play a role in valve function Discharging chambers Pumps of the heart When ventricles contract, blood is propelled out of the heart into circulation: The right ventricle pumps blood into the pulmonary trunk, which routes the blood to the lungs where gas exchange occurs The left ventricle pumps blood into the aorta, the largest artery in the body, to the systemic trunk Slide 22 Ventricles: The Discharging Chambers Slide 23 INTERNAL HEART ANATOMY Slide 24 Pathway of Blood Through the Heart The right side of the heart pumps blood into the pulmonary circuit: Blood returning from the body is relatively oxygen-poor and carbon dioxide-rich Blood enters the right atrium and passes into the right ventricle, which pumps it to the lungs via the pulmonary arteries (conduct blood away from the heart) In the lungs, the blood unloads carbon dioxide and picks up oxygen (oxygenated) The left side of the heart pumps blood into the systemic circuit Slide 25 Pathway of Blood Through the Heart Freshly oxygenated blood from the lungs is carried by the pulmonary veins (toward the heart) back to the left side of the heart Left side of the heart is the systemic circuit Freshly oxygenated blood leaving the lungs is returned to the left atrium and passes into the left ventricle, which pumps it into the aorta The aorta transports blood via smaller arteries to the body tissues, where gases and nutrients are exchanged across the capillary walls Then the blood, once again loaded with carbon dioxide and depleted of oxygen, returns through the systemic veins to the right atrium via the superior vena cava and inferior vena cava Slide 26 Pathway of Blood Through the Heart Although equal volumes of blood are pumped to the pulmonary and systemic circuits at any moment, the two ventricles have unequal work-loads: Pulmonary circuit, served by the right ventricle, is a short, low-pressure circulation Systemic circuit, associated with the left ventricle, takes a pathway through the entire body and encounters about five times as much friction, or resistance to blood flow Slide 27 Ventricles: The Discharging Chambers Slide 28 SYSTEMIC AND PULMONARY CIRCULATION Slide 29 Pathway of Blood Through the Heart Functional differences of the two ventricles are revealed in their anatomy The walls of the left ventricle are three-four times as thick as those of the right ventricle, and its cavity is nearly circular The right ventricular cavity is flattened into a crescent shape that partially encloses the left ventricle, much the way a hand might loosely grasp a clenched fist Consequently, the left ventricle can generate much more pressure than the right and is a far more powerful pump Slide 30 SYSTEMIC AND PULMONARY CIRCULATION Slide 31 Coronary Circulation The heart receives no nourishment from the blood as it passes through the chamber: The myocardium is too thick to make diffusion a practical means of nutrient delivery The coronary circulation provides the blood supply for the heart cells: The arterial supply of the coronary circulation is provided by the right and left coronary arteries, both arising from the base of the aorta and encircling the heart in the atrioventricular groove Slide 32 Coronary Circulation The left coronary artery runs toward the left side of the heart and then divides into its major branches: Anterior interventricular artery : follows the anterior interventricular sulcus and supplies blood to the interventricular septum and anterior walls of both ventricles Circumflex artery: supplies the left atrium and the posterior walls of the left ventricle Slide 33 Coronary Circulation The right coronary artery: courses to the right side of the heart, where it also divides into two branches Marginal artery: serves the myocardium of the lateral right side of the heart Posterior interventricular artery: runs to the heart apex and supplies the posterior ventricular walls Near the apex of the heart, this artery merges (anastomoses) with the anterior interventricular artery Together the branches of the right coronary artery supply the right atrium and nearly all the right ventricle Slide 34 CORONARY CIRCULATION Slide 35 The arterial supply of the heart varies considerably Example: 15% of people, the left coronary artery gives rise to both the anterior and posterior interventricular arteries 4% of people, a single coronary artery supplies the whole heart There may be both right and left marginal arteries There are many anastomoses among the coronary arterial branches: These fusing networks provide additional (collateral) routes for blood delivery to the heart Explains how the heart can receive adequate nutrition even when one of its coronary arteries is almost entirely occluded Even so, complete blockage of a coronary artery leads to tissue death and heart attack Slide 36 CORONARY CIRCULATION After passing through then capillary beds of the myocardium, the venous blood is collected by the cardiac veins, whose paths roughly follow those of the coronary arteries These veins join together to form an enlarged vessel called the coronary sinus, which empties the blood into the right atrium Obvious on the posterior aspect of the heart Slide 37 CORONARY CIRCULATION The sinus has three large tributaries: Great cardiac vein: in the anterior interventricular sulcus Middle cardiac vein: in the posterior interventricular sulcus Small cardiac vein: running along the hearts right inferior margin Additionally, several anterior cardiac veins empty directly into the right atrium anteriorly Slide 38 HOMEOSTATIC IMBALANCE Blockage of the coronary arterial circulation can be serious and sometimes fatal Angina pectoris: Thoracic pain caused by a fleeting deficiency in blood delivery to the myocardium May result from stress-induced spasms of the coronary arteries or from increased physical demands on the heart Myocardial cells are weakened by the temporary lack of oxygen but do not die Myocardial infarction (MI): There is prolonged coronary blockage that leads to cell death Commonly called a heart attack or coronary Because adult cardiac muscle is essentially amitotic, most areas of cell death are repaired with noncontractile scar tissue Whether or not a person survives a myocardial infraction depends on the extent and location of the damage Damage to the left ventricle, which is the systemic pump, is most serious Slide 39 Heart Valves Blood flows through the heart in one direction: from atria to ventricles and out the great arteries leaving the superior aspect of the heart This one-way traffic is enforced by valves that open and close in response to differences in blood pressure on their two side Slide 40 Heart Valves Slide 41 Slide 42 Two atrioventricular (AV) valves, one located at each atrial-ventricular junction ( tricuspid and bicuspid valves) prevent backflow into the atria when the ventricles contract Right AV valve (tricuspid) has three flexible cusps (flaps of endocardium reinforced by connective tissue cores) Left AV valve (bicuspid) has two flexible cusps Commonly called the mitral valve because of its resemblance to the two-sided bishops miter or hat Slide 43 Heart Valves Slide 44 Slide 45 INTERNAL HEART ANATOMY Slide 46 Heart Valves Attached to each AV valve flap are tiny white collagen cords called chordae tendineae (heart strings): Anchor the cusps to the papillary muscles protruding from the ventricular walls Slide 47 HEART VALVES Slide 48 Heart Valves Blood returning to the heart fills atria, putting pressure against AV valve AV valve opens When the heart is relaxed, the AV valves are open hanging limply into the ventricular chambers below and blood flows into the atria and then through the open AV valves into the ventricles When ventricles contracts, compressing the blood in their chambers, the intraventricular pressure rises, forcing the blood superiorly against the valve flaps As a result, the flaps edges meet, closing the AV valve Slide 49 Heart Valves The chordae tendineae and the papillary muscles serve as guy- wires to anchor the valve flaps in their closed position If the cusps were not anchored in this manner, they would be blown upward into the atria, in the same way an umbrella is blown inside out by a gusty wind Slide 50 Heart Valves Slide 51 The aortic and pulmonary semilunar valves are found in the major arteries leaving the heart (aorta and pulmonary trunk) They prevent backflow of blood into the ventricles Each SL valve is fashioned from three pocketlike cusps, each shaped like a crescent moon (half-moon) Mechanism of action differs from that of the AV valves When the ventricles contracts and intraventricular pressure rises above the pressure in the aorta and pulmonary trunk, the SL valves are forced open and their cusps flatten against the arterial walls as blood rushes past them the semilunar valves are open Slide 52 HEART VALVE OPERATION Slide 53 Heart Valves When the ventricles relax, and the blood (no longer propelled forward by the pressure of ventricular contraction) flows backward toward the heart, it fills the cusps and closes the valves Slide 54 HEART VALVE OPERATION Slide 55 Heart Valves There are no valves guarding the entrances of the venae cavae and pulmonary veins into the right and left atria, respectively Small amounts of blood do spurt back into these vessels during atrial contraction, but backflow is minimal because as it contracts, the atrial myocardium compresses ( and collapses) these venous entry points Slide 56 HOMEOSTATIC IMBALANCE Heart valves are simply devices, and the heartlike any mechanical pumpcan function with leaky valves as long as the impairment is not too great Severe valve deformities can seriously hamper cardiac function Incompetent valve: Forces the heart to repump the same blood over and over because the valve does not close properly and blood backflows Valvular stenosis (narrowing): The valve flaps become stiff (typically because of scar tissue formation following endocarditis or calcium salt deposit) and constrict then opening This stiffness compels the heart to contract more forcibly than normal Hearts work load increases Heart may be severely weakened Valve replacement: Synthetic valve Pig heart valve chemically treated to prevent rejection Cryopreserved valves from human cadavers Tissue-engineered polymer valves Slide 57 CARDIAC MUSCLE CELLS Cardiac muscle (like skeletal muscle) is striated and contraction occurs via the sliding filament mechanism In contrast to skeletal muscle, cardiac muscle is short, fat, branched Intercellular spaces are filled with a loose connective tissue matrix containing numerous capillaries Slide 58 CARDIAC MUSCLE CELLS Plasma membranes of adjacent cardiac cells interlock like the ribs of two sheets of corrugated cardboard (intercalated discs) Disc contain anchoring desmosomes and gap junctions: Desmosomes prevent adjacent cells from separating during contraction Gap junctions allow ions to pass from cell to cell Large mitochondria account for about 25% of the volume of the cardiac cell (compared with only about 2% in skeletal muscle) Gives cardiac cells a high resistance to fatigue Slide 59 Mechanism and Events of Contraction 1. Means of stimulation: Some cardiac muscle cells are s elf-excitable and can initiate their own depolarization in a spontaneous and rhythmic way 2. Organ versus motor unit contraction Skeletal muscle: All cells of a given motor unit (but not the entire muscle) are stimulated and contract at the same time Impulses do not spread from cell to cell Cardiac muscle: The heart contracts as unit or not at all Transmission of the depolarization wave across the heart from cell to cell via ion passage through gap junctions, which tie all cardiac muscle cells together into a single contractile unit Slide 60 Mechanism and Events of Contraction 3. Length of absolute refractory period: Refractory period: repolarization period in which the cell cannot be stimulated again until repolarization is complete Repolarization: movement of the membrane potential to the initial resting (polarized) state The hearts absolute refractory period (the inexcitable period when Na + channels are still open or are closed or inactivated) is longer than a skeletal muscles preventing tetanic contractions (smooth, continues contraction without any evidence of relaxation) Long cardiac refractory period normally prevents tetanic contractions, which would stop the hearts pumping action 250ms in cardiac muscle (nearly as long as the contraction) 1-2 ms in skeletal muscle (contraction last 20 to 100ms) Slide 61 Membrane Potential and Membrane Permeability during Action Potentials of Contractile Cardiac Muscle Cells (a) relationship between the action potential, period of contraction, and absolute refractory period in a single ventricular cell Slide 62 Membrane Potential and Membrane Permeability during Action Potentials of Contractile Cardiac Muscle Cells (b) Membrane permeability changes during the action potential (The Na + permeability rises to a point off the scale during the action potential) Slide 63 Membrane Potential and Membrane Permeability during Action Potentials of Contractile Cardiac Muscle Cells Influx of Na + from the extracellular fluid into cardiac cells initiates a positive feedback cycle that causes the rising phase of the action potential (-90 mV to nearly + 30 mV) by opening voltage-regulated fast Na + channels Period of increased Na + permeability is very brief, because the sodium gates are quickly inactivated and the Na + channels close Slide 64 Membrane Potential and Membrane Permeability during Action Potentials of Contractile Cardiac Muscle Cells Transmission of the depolarization causes causes the sarcoplasmic reticulum to release Ca 2+ into the sarcoplasm (cytoplasm) Ca 2+ provides the signal for cross bridge activation Slide 65 Membrane Potential and Membrane Permeability during Action Potentials of Contractile Cardiac Muscle Cells Although Na + permeability has plummeted to its resting levels and repolarization has begun by this point, the calcium surge across the membrane prolongs the depolarization potential tracing (a) At the same time, K + permeability decreases, which also prolongs the plateau and prevents rapid repolarization As long as Ca 2+ is entering, the cells continue to contract Notice in (a) that muscle tension develops during the plateau, and peaks just after the plateau ends Slide 66 Membrane Potential and Membrane Permeability during Action Potentials of Contractile Cardiac Muscle Cells After about 200ms, the slope of the action potential tracing falls rapidly This results from closure of Ca 2+ channels, Ca 2+ transport from the cytosol into the extracellular space or SR (or mitochondria), and opening of voltage- regulated K + channels, which allows a rapid loss of potassium from the cell that restores the resting membrane potential During repolarization, Ca 2+ is pumped back into the SR and the extracellular space Slide 67 Energy Requirements Cardiac muscle has more mitochondria than skeletal muscle does, reflecting its greater dependence on oxygen for its energy metabolism The heart relies exclusively on aerobic respiration for its energy demands (skeletal muscle during oxygen deficits can carry out anaerobic respiration) Cardiac muscle cannot incur much of an oxygen debt and still operate effectively Cardiac muscle is capable of switching nutrient pathways to use whatever nutrient supply is available Thus, the real danger of an inadequate blood supply to the myocardium is lack of oxygen, not of nutrient fuels Slide 68 HOMEOSTATIC IMBALANCE When a region of heart muscle is deprived of blood (is Ischemic), the oxygen-starved cells begin to metabolize anaerobically, producing lactic acid The rising H + level that results hinders the cardiac cells ability to produce the ATP they need to pump Ca 2+ into the extracellular fluid The resulting increase in intracellular H + and Ca 2+ levels causes the gap junctions (which are usually open) to close, electrically isolating the damaged cells and forcing generated action potentials to find alternate routes to the cardiac cells beyond them If the ischemic area is large, the pumping activity of the heart as a whole may be severely impaired, leading to a heart attack Slide 69 HEART PHYSIOLOGY Electrical Events: Intrinsic conduction system is made up of specialized cardiac cells that initiate and distribute impulses, ensuring that the heart depolarizes in an orderly fashion Even if all nerve connections to the heart are severed, the heart continues to best Slide 70 HEART PHYSIOLOGY The autorhythmic cells have an unstable resting potential, called pacemaker potentials, that continuously depolarizes The mechanism of the pacemaker potential is believed to result from gradually reduced membrane permeability to K + Then, because Na + permeability is unchanged and Na + continues to diffuse into the cell at a slow rate, the balance between K + loss and Na + entry is upset and the membrane interior becomes less and less negative (more positive) Slide 71 HEART PHYSIOLOGY Ultimately, at threshold (approximately -40 mV), fast Ca 2+ channels open, allowing explosive entry of Ca 2+ (as well as some Na + ) from the extracellular space Thus, in autorhythmic cells, it is the influx of Ca 2+ (rather than Na + ) that produces the rising phase of the action potential and reverses the membrane potential Once repolarization is complete, K + channels are inactivated, K + permeability declines, and the slow depolarization to threshold begins again Slide 72 Pacemaker and Action Potentials of Autorhythmic Cells of the Heart Slide 73 HEART PHYSIOLOGY Autorhythmic cardiac cells are found in the following areas: Sinoatrial node Atrioventricular node Atrioventricular bundle Right and left bundle branches Ventricular walls (Purkinje fibers) Slide 74 HEART PHYSIOLOGY Impulses pass across the heart in the same order: sinoatrial node, atrioventricular node, atrioventricular bundle, right and left bundle branches, and Purkinjie fibers Slide 75 The intrinsic conduction system of the heart and succession of the action potential through selected areas of the heart during one heartbeat Slide 76 Sequence of Excitation Sinoatrial node (SA): Pacemaker: Located in the right atrium wall, just inferior to the entrance of the superior vena cava Typically generates impulses about 75 times every minute Its inherent rate in the absence of extrinsic neural and hormonal factors is closer to 100 times per minute Sets the pace for the heart Its characteristic rhythm (sinus rhythm) determines heart rate Slide 77 Sequence of Excitation Atrioventricular node: From the SA node, the depolarization wave spreads via gap junctions throughout the atria and via the internodal pathway to the atrioventricular (AV) node, located in the inferior portion of the interatrial septum immediately above the tricuspid valve Slide 78 Sequence of Excitation Atrioventricular bundle: From the AV node, the impulse sweeps to the atrioventricular bundle (bundle of His) in the superior oart of the interventricular septum Although the atria and ventricles abut each other, they are not connected by gap junctions The AV bundle is the only electrical connection between them The balance of the AV junction is insulated by the nonconducting fibrous skeleton of the heart Slide 79 Sequence of Excitation Right and Left Bundle Branches: The AV bundle persists only briefly before splitting into two pathwaysthe right and left bundle branches which course along the interventricular septum toward the heart apex Slide 80 Sequence of Excitation Purkinje Fibers: Long strands of barrel-shaped cells with few myofibrils Complete the pathway through the interventricular septum, penetrate into the apex, and then turn superiorly into the ventricular walls Bulk of ventricular depolarization depends on these fibers and, ultimately, on cell-to-cell transmission of the impulses via gap junctions between the ventricular muscle cells Because the left ventricle is much larger than the right, the fibers are more elaborate in the left ventricle Directly supply the papillary muscles which are excited to contract before the rest of the ventricular muscles Slide 81 Sequence of Excitation The total time between initiation of an impulse by the SA node and depolarization of the last of the ventricular muscle cells is approximately 0.22 s (220 ms) in a healthy human heart A wringing contraction begins at the heart apex and moves toward the atria, following the direction of the excitation wave through the ventricle walls This ejects some of the contained blood superiorly into the large arteries leaving the ventricles Slide 82 HOMEOSTATIC IMBALANCE Arrhythmias: Uncoordinated atria and ventricular contractions Fibrillation: Condition of rapid and irregular or out-of-phase contractions in which control of heart rhythm is taken away from the SA node by rapid activity in other heart regions Compared to a squirming bag of worms Fibrillating ventricles are useless as pumps Unless defibrillated, circulation stops and brain death occurs Accomplished by electrically shocking the heart Depolarizes the entire myocardium (hope is: the slate is wiped clean) SA node will begin to function normally and sinus rhythm reestablished Implantable cardioverter defibrillators (ICDs) Slows an abnormally fast heart or emits an electrical shock if the heart begins to fibrillate Slide 83 Defibrillator Slide 84 Slide 85 Slide 86 Slide 87 HOMEOSTATIC IMBALANCE A small region of the heart becomes hyperexcitable, sometimes as a result of too much caffeine or nicotine, and generates impulses more quickly than the SA node Leads to premature contractions (extrasystole) Heart Block: A blockage that interferes with the impulse transmission route from atria to ventricle Interferes with the ability of the ventricles to receive pacing impulses In total heart block no impulses get through and the ventricles beat at their intrinsic rate, which is too slow to maintain adequate circulation A fixed-rate artificial pacemaker, set to deliver impulses at a constant rate, is usually implanted Those suffering from partial block, in which some of the atrial impulses reach the ventricles, commonly receive demand-type pacemakers, which deliver impulses only when the heart is not transmitting on its own Slide 88 PACEMAKERS Slide 89 Slide 90 PACEMAKER Slide 91 Slide 92 Extrinsic Innervation of the Heart Although the basic heart rate is set by the intrinsic conduction system, fibers of the autonomic nervous system modify the beat and introduce a subtle variability from one beat to the next The autonomic nervous system modifies the heartbeat: Sympathetic center increases rate and depth of the heartbeat Parasympathetic center slows the heartbeat Slide 93 Extrinsic Innervation of the Heart Cardiac centers are located in the medulla oblongata Sympathetic (Cardioacceleratory Center) projects to motor neurons in the T 1 -T 5 level of the spinal cord Innervate with the SA and AV nodes, heart muscle, and the coronary arteries Stimulates heart rate Parasympathetic (Cardioinhibitory Center) sends impulses to the dorsal vagus nucleus in the medulla, which in turn sends inhibitory impulses to the heart via branches of the vagus nerves Project most heavily to the SA and AV nodes Slows heart rate Slide 94 Autonomic innervation of the Heart Slide 95 Electrocardiography The electrical currents generated in and transmitted through the heart spread throughout the body and can be amplified with an electrocardiograph Graphic recording of heart activity obtained is called an electrocardiogram (ECG or EKG) An ECG is a composite of all of the APs (action potentials) generated by nodal and contractile cells at a given time and not, as sometimes assumed, a tracing of a single AP Typically 12 leads used (positioned at various sites on the body surface) 3 are bipolar (two poles: AC current ?) leads that measure the voltage difference either between the arms or between an arm and a leg 9 are unipolar (one pole) leads Together the 12 leads provide a fairly comprehensive picture of the hearts electrical activity Slide 96 Electrocardiography Slide 97 A typical ECG has three distinguishable waves called deflection waves Small P wave: Lasts about 0.08 s Results from movement of the depolarization wave from the SA node through the atria Approximately 0.1 s after the P wave begins, the atria contract Slide 98 The sequence of excitation of the heart related to the deflection waves of an ECG tracing Slide 99 Electrocardiography P-Q interval: The time from the beginning of atrial excitation to the beginning of ventricular excitation About 0.16 s Sometimes called the P-R interval because the Q wave tends to be very small It includes atrial depolarization (and contraction) as well as the passage of the depolarization wave through the rest of the conduction system Slide 100 The sequence of excitation of the heart related to the deflection waves of an ECG tracing Slide 101 Electrocardiography The large QRS complex: Results from ventricular depolarization and precedes ventricular contraction It has a complicated shape because the paths of the depolarization waves through the ventricular walls change continuously, producing corresponding changes in current direction Average duration is 0.08 s Slide 102 The sequence of excitation of the heart related to the deflection waves of an ECG tracing Slide 103 Electrocardiography S-T segment: Action potential is in its plateau phase Entire ventricular myocardium is depolarized Slide 104 Electrocardiography The T wave: Caused by ventricular repolarization Typically lasts about 0.16 s Repolarization is slower than depolarization T wave is more spread out and has a lower amplitude (height) than the QRS wave Because atrial repolarization takes place during the period of ventricular excitation, the wave representing atrial repolarization is normally obscured by the large QRS complex being recorded at the same time Slide 105 Electrocardiography Q-T interval: Lasting about 0.8 s Period from the beginning of ventricular depolarization through ventricular repolarization Slide 106 Electrocardiography Slide 107 In a healthy heart, the size, duration, and timing of the deflection waves tend to be consistent Changes in the pattern or timing of the ECG may reveal a diseased or damaged heart or problems with the hearts conduction system Slide 108 Electrocardiography An enlarged R wave: hints of enlarged ventricles Flattened T wave: indicates cardiac ischemia (deficient blood flow) Prolonged Q-T interval: reveals are polarization abnormality that increases the risk of ventricular arrhythmias Slide 109 ELECTROCARDIOGRAM Slide 110 Normal and Abnormal ECG Tracings a: Normal sinus rhythm b: Junctional rhythm: SA node nonfunctional P waves absent Heart rate paced by AV node at 40-60 beats/min Slide 111 Normal and Abnormal ECG Tracings c: Second degree heart block: Some P waves not conducted through AV node More P than QRS waves Where P waves are conducted normally, the P:QRS ratio is 1:1 In total heart block, there is no whole number ratio between P and QRS waves, and the ventricles are no longer paced by the SA node Slide 112 Normal and Abnormal ECG Tracings d: Ventricular fibrillation: Chaotic, grossly irregular, bizarre ECG deflections Acute heart attack and electric shock Slide 113 HEART SOUNDS Normal: two sounds (lub-dub) The basic rhythm of the heart sounds is lub-dup, pause, lub-dup, pause, and so on, with the pause indicating the quiescent period The first heart sound, lub, corresponds to closure of the AV valves Signifies the beginning of systole when ventricular pressure rises above atrial pressure Tends to be louder, longer, and more resonant than the second The second heart sound, dup, corresponds to the closure of the semilunar valves Short, sharp sound Beginning of ventricular diastole Slide 114 Summary of events occurring in the Heart during the Cardiac Cycle Slide 115 HEART SOUNDS Because the mitral valve closes slightly before the tricuspid valve does, and the aortic SL valve generally snaps shut just before the pulmonary valve, it is possible to distinguish the individual valve sounds by auscultating (listening for sounds within the body) four specific regions of the thorax Notice that these four points, while not directly superficial to the valves (because the sounds take oblique paths to reach the chest wall), do define the four corners of the normal heart Knowing normal heart size and location is essential for recognizing an enlarged (and often diseased) heart Slide 116 HEART SOUNDS Slide 117 HOMEOSTATIC IMBALANCE Abnormal Heart Sounds: blood flows silently as long as the flow is smooth and uninterrupted If it strikes obstructions, its flow becomes turbulent Heart murmurs are extraneous heart sounds due to turbulent backflow of blood through a valve that does not close tightly Fairly common in young children and some elderly people with perfectly healthy hearts Probably because their heart walls are relatively thin and vibrate with rushing blood Most often, murmurs indicate valve problems Incompetent valve: Swishing sound is heard as the blood backflows or regurgitates through the partially open valve, after the valve has (supposedly) closed Stenotic valve: Valve opening is narrowed Restricts blood flow through the valve High pitched sound or click can be detected when the valve should be wide open during systole, but is not Slide 118 Mechanical Events: The Cardiac Cycle Cardiac Cycle: Includes all events associated with the blood flow through the heart during one complete heartbeat, that is, atrial systole and diastole followed by ventricular systole and diastole Systole is the contractile phase of the cardiac cycle Diastole is the relaxation phase of the cardiac cycle Marked by a succession of pressure and blood volume changes in the heart Cardiac Cycle: Ventricular Filling: Mid-to-Late Diastole Ventricular Systole Isovolumetric Relaxation: Early Diastole Slide 119 (1) Ventricular Filling Mid-to-late diastole Pressure in the heart is low Blood returning from the circulation is flowing passively through the atria and the open AV valves into the ventricles Aortic and pulmonary semilunar valves are closed 70% of ventricular filling occurs during this period The remaining 30% is delivered to the ventricles when the atria contract toward the end of this phase AV valve flaps begin toward the closed position NOW the stage is set for atrial systole Following depolarization (P wave of ECG) The atria contract, compressing the blood in their chambers Causes a rise in atria pressure, which propels residual blood out of the atria into the ventricles At this point the ventricles are in the last part of their diastole and have the maximum volume of blood Then the atria relax and the ventricles depolarize (QRS complex) Slide 120 Summary of events occurring in the Heart during the Cardiac Cycle Slide 121 (2a) Ventricular Systole As the atria relax, the ventricles begin contracting Ventricular pressure rises, closing the AV valves Isovolumetric contraction phase: for a split second, the ventricles are completely closed chambers and blood volume in the chambers remains constant Slide 122 Summary of events occurring in the Heart during the Cardiac Cycle Slide 123 (2b) Ventricular Systole Ventricular pressure continues to rise and when it finally exceeds the pressure in the large arteries issuing from the ventricles, the isovolumetric stage ends as the SL valves are forced open and blood is expelled from the ventricles into the aorta and pulmonary trunk (ventricular ejection phase) Pressure in the aorta normally reaches about 120 mm Hg Slide 124 Summary of events occurring in the Heart during the Cardiac Cycle Slide 125 (3) Isovolumetric Relaxation Early diastole Brief phase following the T wave Ventricles relax Blood remaining in their chambers is no longer compressed Ventricle pressure drops Blood in the aorta and pulmonary trunk backflows toward the heart, closing the SL valves Closure of the Aortic SL valve causes a brief rise in aortic pressure as backflowing blood rebounds off the closed valve cusps (dicrotic notch) Ventricles are totally closed Slide 126 Summary of events occurring in the Heart during the Cardiac Cycle Slide 127 (a) An ECG tracing correlated with graphs of pressure and volume changes. Time occurrence of heart sounds is also indicated. Slide 128 Mechanical Events: The Cardiac Cycle All during ventricular systole, the atria have been in diastole; they have been filling with blood and the intra-atrial pressure has been rising When blood pressure on the atrial side of the AV valves exceeds that in the ventricles, the AV valves are forced open and ventricular filling, phase 1, begins again Atrial pressure drops to its lowest point and ventricular pressure begins to rise, completing the cycle Slide 129 Summary of events occurring in the Heart during the Cardiac Cycle Slide 130 Mechanical Events: The Cardiac Cycle Average heart beats: 75 beats / minute 4500 beats / hour 108,000 beats / day 39,420,000 beats / year 709,560,000 beats / 18 years 2,759,400,000 beats / 70 years Slide 131 Mechanical Events: The Cardiac Cycle Two important points: 1. Blood flow through the heart is controlled entirely by pressure changes 2. Blood flows down a pressure gradient through any available opening The pressure changes, in turn, reflect the alternating contraction and relaxation of the myocardium and cause the heart valves to open, which keeps blood flowing in the forward direction The pulmonary circulation is a low-pressure circulation as evidenced by the much thinner myocardium of its right ventricle Systemic aortic pressure: 120 mm Hg (systolic) and 80 mm Hg (diastolic) Pulmonary artery pressure: 24 mm Hg (systolic) and 8 mm Hg (diastolic) Slide 132 CARDIAC OUTPUT (CO) The amount of blood pumped out by each ventricle in 1 minute Stroke Volume is defined as the volume of blood pumped out of a ventricle per beat Calculated as the product of stroke volume (SV) and heart rate (HR) CO = HR x SV CO = 75 beats / min x 70 ml / beat CO = 5250 ml / min (5.25 L / min) The normal adult blood volume is about 5 L (1.32 gallons) Thus, the entire blood supply passes through each side of the heart once each minute Slide 133 Regulation of Stroke Volume Preload The Frank-Starling law of the heart states that the critical factor controlling stroke volume is the degree of stretch of cardiac muscle cells immediately before they contract Stretching cardiac cells can produce dramatic increases in contractile force The most important factor stretching cardiac muscle is the amount of blood returning to the heart and distending its ventricles Slide 134 (a) Preload is related to the amount of blood stretching the ventricular fibers just before systole Slide 135 CARDIAC OUTPUT Slide 136 Regulation of Stroke Volume Contractility Defined as an increase in contractile strength that is independent of muscle stretch end systolic volume The more vigorous contractions are a direct consequence of Ca 2+ influx into the cytoplasm from extracellular fluid and the SR (sarcoplasmic reticulum) Enhanced contractility results in ejection of more blood from the heart: Result of increased sympathetic stimulation of the heart Increased Ca 2+ promotes more cross bridge binding (actin and myosin) and enhances ventricular contractility Slide 137 Regulation of Stroke Volume Contractility Factors that increase contractility: positive inotropic: Calcium Hormones: Glucagon Thyroxine Epinephrine Drug: digitalis Slide 138 Regulation of Stroke Volume Contractility Factors that impair or decrease contractility: negative inotropic: Acidosis: excess H + Rising extracellular K + Drugs: Calcium channel blockers Slide 139 CARDIAC OUTPUT Slide 140 Regulation of Stroke Volume Afterload Ventricular pressure that must be overcome before blood can be ejected from the heart It is essentially the back pressure exerted on the aortic and pulmonary valves by arterial blood 80mm Hg in the aorta 8 mm Hg in the pulmonary artery Normal individual: not a major concern Individual with hypertension: it reduces the ability of the ventricles to eject blood: More blood remains in the heart after systole, resulting in increased end systolic volume (ESV) and reduced stroke volume Slide 141 (b) Afterload is the pressure that the ventricles must overcome to force open the aortic and pulmonary valves Slide 142 Preload and Afterload influence Stroke Volume Slide 143 CARDIAC OUTPUT Slide 144 Regulation of Heart Rate A healthy cardiovascular system, SV tends to be relatively constant When blood volume drops or heart is weakened: SV declines and CO is maintained by increasing HR and contractility Sympathetic stimulation of pacemaker cells increases heart rate and contractility, while parasympathetic inhibition of cardiac pacemaker cells decreases heart rate Epinephrine, thyroxine, and calcium influence heart rate Slide 145 Autonomic Nervous System Regulation Extrinsic controls affecting heart rate When sympathetic nervous system is activated by emotional or physical stressors, such as fright, anxiety, or exercise: Sympathetic nerve fibers release norepinephrine at their cardiac synapses Binds to beta adrenergic receptors in the heart Pacemaker fires more rapidly Heart responds by beating faster Slide 146 CARDIAC OUTPUT Slide 147 Autonomic Nervous System Regulation Sympathetic stimulation also enhances contractility by enhancing Ca 2+ entry into contractile cells Slide 148 Mechanism by which Norepinephrine influences Heart contractility Slide 149 Autonomic Nervous System Regulation The parasympathetic division opposes sympathetic effects and effectively reduces heart rate when a stressful situation has passed May be persistently activated in certain emotional conditions, such as grief and severe depression Responses are mediated by acetylcholine, which hyperpolarizes the membranes of its effector cells by opening K + channels Slide 150 Autonomic Nervous System Regulation Under resting conditions, both autonomic divisions continuously send impulses to the SA node of the heart, but the dominant influence is inhibitory Exhibits vagal tone Heart rate is generally slower than it would be if the vagal nerves were not innervating it Cutting the vagal nerves results in an almost immediate increase in heart rate of about 25 beats / min Slide 151 Chemical Regulation Hormones: Epinephrine: liberated by the adrenal medulla during sympathetic nervous system activation Produces the same effect as does norepinephrine released by the sympathetic nerves Enhances heart rate and contractility Thyroxine: thyroid gland hormone that increases metabolic rate and body heat production Causes a slower but more sustained increase in heart rate than that caused by epinephrine Slide 152 Chemical Regulation Ions: Physiological relationships between intracellular and extracellular ions must be maintained for normal heart function Plasma electrolyte imbalance pose real dangers to the heart Slide 153 HOMEOSTATIC IMBALANCE Hypocalcemia: reduced Ca 2+ blood levels Depress the heart Hypercalcemia: above-normal levels of Ca 2+ Prolong the plateau phase of action potential Dramatically increase heart irritability Lead to spastic (abnormal muscle contraction) heart contractions that permit little rest Excess Na + and K + are equally dangerous Hypernatremia : excessive Na + Inhibits transport of Ca 2+ into the cardiac cells, thus blocking heart contraction Hyperkalalemia: excessive K + Interferes with depolarization by lowering the resting potential, and may lead to heart block and cardiac arrest Hypokalemia: low K + Is also life threatening, in that the heart beats feebly and arrhythmically Slide 154 HOMEOSTATIC IMBALANCE Age: Fetus: 140-160 beats/min Gradually declines throughout life Gender: Females: 72-80 beats/min Male: 64-72 beats/min Exercise: Raises HR by acting through the sympathetic nervous system Increases systemic blood pressure and routes more blood to the working muscles Trained athletes HR may be as slow as 40 beats/min Body Temperature: Increases HR by enhancing the metabolic rate of cardiac muscle Exercising muscle generate heat: increase HR Cold: decreases HR Slide 155 HOMEOSTATIC IMBALANCE Tachycardia: abnormally fast heart rate (more than 100 beats/min) Occasionally promotes fibrillation (irregular electrical activity in the heart) Considered pathological (due to a disease) Bradycardia: heart rate slower than 60 beats/min Desirable, consequence of endurance training BUT, persistent in poorly conditioned people may result in grossly inadequate blood circulation to body tissues Frequent warning of brain edema (excessive amount of fluid) after head trauma Slide 156 Homeostatic Imbalance of Cardiac Output The hearts pumping action ordinarily maintains a balance between cardiac output and venous return Cogestive Heart Failure: Occurs when the pumping efficiency of the heart is so low that blood circulation cannot meet tissue needs Reflects weakening of the myocardium by various conditions which damage it in different ways: 1. Coronary Atherosclerosis 2. Persistent High Blood Pressure 3. Multiple Myocardial Infarcts 4. Dilated Cardiomyopathy (DCM) Slide 157 (1) Coronary Atherosclerosis Clogging of the coronary vessels with fatty buildup Heart becomes increasingly hypoxic (inadequate oxygen) and begins to contract ineffectively Slide 158 (2) Persistent High Blood Pressure Aortic pressure is normally 80mm Hg during diastole When aortic diastolic blood pressure rises to 90 mm Hg or more, the myocardium must exert more force to open the aortic valve and pump out the same amount of blood Myocardium hypertrophies (increased size of tissue / organ) Stress takes its toll and the myocardium becomes progressively weaker Slide 159 (3) Multiple Myocardial Infarcts Infarct: region of dead, deteriorating tissue resulting from a lack of blood supply Succession of MIs depress pumping efficiency because the dead heart cells are replaced by noncontractile fibrous (scar) tissue Slide 160 (4) Dilated Cardiomyopathy (DCM) Ventricles stretch and become flabby and the myocardium deteriorates Cause often unknown Drug toxicity (alcohol, cocaine, excess catecholamines, chemotherapeutic agents), hypothyroidism, and inflammation of the heart are implicated in some cases, as is congestive heart failure The hearts attempts to work harder result in increasing levels of Ca 2+ in the cardiac cells which activates a calcium-sensitive enzyme that initiates a cascade which switches on genes that cause heart enlargement Because ventricular contractility is impaired, CO is poor and the condition progressively worsens Slide 161 Pulmonary Congestion Pulmonary congestion occurs when the left side of the heart fails, resulting in pulmonary edema: Right side of the heart continues to pump blood to the lungs Left side does not adequately eject the returning blood into the systemic circulation Blood vessels in the lungs become engorged with blood, pressure in them increases, and fluid leaks from the circulation into the lung tissue, causing pulmonary edema Slide 162 Peripheral Congestion If the right side of the heart fails, peripheral congestion occurs Blood stagnates in body organs, and pooled fluids in the tissue spaces impair the ability of body cells to obtain adequate amounts of nutrients and oxygen and to rid themselves of wastes Resulting edema is most noticeable in the extremities (feet, ankles, and fingers) Slide 163 DEVELOPMENTAL ASPECTS OF THE HEART Embryological Development: The heart begins as a pair of endothelial tubes that fuse to make a single heart tube with four bulges representing the four chambers The foramen ovale is an opening in the interatrial septum that allows blood returning to the pulmonary circuit to be directed into the atrium of the systemic circuit (bypass the pulmonary circuit and the collapsed, nonfunctional fetal lungs) The ductus arteriosus is a vessel extending between the pulmonary trunk to the aortic arch that allows blood in the pulmonary trunk to be shunted to the aorta (bypass the lungs) Slide 164 EMBRYONIC DEVELOPMENT Slide 165 EXAMPLES of CONGENITAL HEART DEFECTS Purple indicates heart areas where the defects are present Slide 166 HEART DEVICES Slide 167 DEVELOPMENTAL ASPECTS OF THE HEART Aging Aspects of the Heart Sclerosis and thickening of the valve flaps occurs over time, in response to constant pressure of the blood against the valve flaps Decline in cardiac reserve occurs due to a decline in efficiency of sympathetic stimulation Fibrosis of cardiac muscle may occur in the nodes of the intrinsic conduction system, resulting in arrhythmias Atherosclerosis is the gradual deposit of fatty plaques in the walls of the systemic vessels