the heart

The Circulatory System: Heart Chapter 19 Overview of the Cardiovascular System  Cardiology : is the study of the heart and its disorders  Cardiovascular system: consists of heart and blood vessels  Heart : is a pump that keeps blood flowing through the vessels  Vessels: deliver blood to body tissues and returns it to the heart  Arteries: all vessels that carry blood away from heart  Veins: all vessels that carry blood toward heart  Capillaries: microscopic vessels that connect the smallest arteries to the smallest veins  Circulatory system: refers to heart, vessels, and blood The Pulmonary and Systemic Circuits  Cardiovascular system has two major divisions:  Pulmonary circuit: carries blood to lungs for gas exchange and back to heart  Systemic circuit: supplies oxygenated blood to all tissues of the body and returns it to the heart  Right side of heart supplies the pulmonary circuit  Oxygen-poor blood arrives from body tissues  Blood sent to alveoli of lungs via pulmonary trunk and pulmonary arteries, picks up oxygen, and returns to heart via pulmonary veins  Left side of heart of heart supplies the systemic circuit:  Fully oxygenated blood sent to body tissues via aorta, which branches into smaller vessels  Blood releases oxygen at the tissues; deoxygenated blood returns to heart via superior vena cava and inferior vena cava  The major arteries and veins entering and leaving the heart are called the great vessels  Which of the following carry oxygen-poor blood? 1. Pulmonary veins and vena cavae 2. Aorta and pulmonary veins 3. Aorta and vena cavae 4. Venae cavae and pulmonary arteries 5. Pulmonary veins and pulmonary arteries Position, Size, and Shape of the Heart  Heart located in mediastinum—space between lungs  Shape of heart:  Base:wide, superior portion of heart, large vessels attach here  Apex: tapered inferior end, tilts to the left  Size of heart:  In adult: weighs 10 ounces, 3.5 in. wide at base, 5 in. from base to apex  At any age, heart is size of fist The Pericardium  Heart enclosed by the pericardium: a double-walled sac  Allows heart to beat without friction, provides room to expand, yet resists excessive expansion  Anchored to diaphragm inferiorly and sternum anteriorly  Structure of pericardium:  Fibrous pericardium—outermost layer; tough, fibrous sac  Serous pericardium:  Parietal layer of the serous pericardium—lines fibrous pericardium  Visceral layer of the serous pericardium (epicardium)—adheres to heart surface and outermost layer of heart itself  Pericardial cavity: space between parietal and visceral layers of serous pericardium, filled with 5 to 30 mL of pericardial fluid  Pericarditis: inflammation of the pericardium; may result in friction rub The Heart Wall  The heart wall has three layers:  epicardium, myocardium, and endocardium  Epicardium (visceral layer of serous pericardium):  Serous membrane covering heart. Adipose in thick layer in some places. Coronary blood vessels travel through this layer  Endocardium :  Smooth inner lining of heart and blood vessels  Myocardium:  Layer of cardiac muscle, thickness is proportional to workload  Fibrous skeleton:  Framework of collagenous and elastic fibers. Provides structural support and attachment for cardiac muscle and anchor for valve tissue (fibrous rings)  Electrical insulation between atria and ventricles; important in timing and coordination of contractile activity The Chambers  The heart has four chambers:  two atria and two ventricles  Right and left atria: Two superior chambers that receive blood returning to the heart; separated from each other by interatrial septum  Each has an associated auricle—an earlike flap that increases the chamber volume  Thin, flaccid walls; pump blood to the ventricles  Right and left ventricles: Two inferior chambers that eject blood into the arteries; separated from each other by interventricular septum  Left ventricle wall is 2-4x thicker than right ventricle, which reflects its greater workload in pumping blood to the entire body (vs to the lungs)  Both ventricles contain trabeculae carneae—internal muscular ridges; help chambers expand and refill more easily The Valves  Valves : ensure one-way flow of blood through heart  Each valve has two or three fibrous flaps—cusps or leaflets  Atrioventricular (AV) valves: control blood flow between atria and ventricles  Right AV (tricuspid): valve usually has three cusps  Left AV valve (mitral valve): usually has two cusps  Tendinous cords (chordae tendineae): strings of connective tissue that attach valve cusps to papillary muscles on floor of ventricle  Prevent AV valves from flipping or bulging into atria when ventricles contract  Semilunar valves: control flow from ventricles into great arteries:  Pulmonary valve: controls the opening between right ventricle and pulmonary trunk  Aortic valve: controls the opening between left ventricle and aorta  During ventricular contraction and blood ejection, cusps pressed up against arterial walls  When ventricles relax, blood flows back toward ventricles and fills cusps, causing valves to close Blood Flow Through the Chambers  Pathway of blood from right atrium, through body, and back to the starting point:  Blood enters right atrium from superior and inferior venae cavae.  Blood in right atrium flows through right AV valve into right ventricle.  Contraction of right ventricle forces pulmonary valve open.  Blood flows through pulmonary valve into pulmonary trunk  Blood is distributed by right and left pulmonary arteries to the lungs, where it unloads carbon dioxide and loads oxygen.  Blood returns from lungs via pulmonary veins to left atrium.  Blood in left atrium flows through left AV valve into left ventricle.  Contraction of left ventricle (simultaneous with step 3) forces aortic valve open.  Blood flows through aortic valve into ascending aorta.  Blood in aorta is distributed to every organ in the body, where it unloads oxygen and loads carbon dioxide.  Blood returns to right atrium via venae cavae. The Coronary Circulation  Heart has its own supply of vessels to deliver blood to myocardium—the coronary circulation  Arterial supply:  Left coronary artery (LCA) branches off ascending aorta  Anterior interventricular branch [left anterior descending (LAD) branch]  Supplies blood to both ventricles and anterior two-thirds of the interventricular septum  Circumflex branch  Passes around left side of heart in coronary sulcus  Gives off left marginal branch and then ends on the posterior side of the heart  Supplies left atrium and posterior wall of left ventricle  Right coronary artery (RCA) branches off the ascending aorta  Supplies lateral aspect of right atrium and ventricle  Posterior interventricular branch  Supplies blood to posterior walls of both ventricles and interventricular septum Angina and Heart Attack  Angina pectoris: chest pain from partial obstruction of coronary blood flow  Pain caused by ischemia of cardiac muscle  Obstruction partially blocks blood flow; myocardium shifts to anaerobic fermentation, producing lactate and thus stimulating pain  Myocardial infarction (MI): sudden death of a patch of myocardium resulting from long-term obstruction of coronary circulation  Atheroma (blood clot or fatty deposit) often obstructs coronary arteries; cardiac muscle downstream of the blockage dies  Heavy pressure or squeezing pain radiating into the left arm  Some painless heart attacks may disrupt electrical conduction pathways, leading to fibrillation and cardiac arrest Cardiac Muscle and the Cardia Conduction System  Heartbeat is myogenic: signal originates in the heart itself  Heart is autorhythmic: has built-in pacemaker and electrical system, so does not rely on nervous system for its rhythm Structure of Cardiac Muscle  Heart: is composed of cardiac muscle; striated like skeletal muscle, but many different features  Cardiomyocytes are striated, short, thick, branched muscle cells; one central nucleus surrounded by light-staining mass of glycogen; sarcoplasmic reticulum lacks terminal cisterns; large T tubules  Intercalated discs: connections between cardiomyocytes; contain interdigitating folds, mechanical junctions, and electrical junctions  Structure of intercalated discs:  Interdigitating folds: membranes of cells folded to lock cells together and increase surface are of contact  Mechanical junctions:  Fascia adherens  Desmosomes  Electrical junctions:  gap junctions allow ions to flow between cells; cells stimulate neighbors and contract in unison Metabolism of Cardiac Muscle  Cardiac muscle depends almost exclusively on aerobic respiration to make ATP  Rich in myoglobin and glycogen  Huge mitochondria: fill 25% of cell  Fatigue resistant because it makes little use of anaerobic fermentation or oxygen debt mechanisms; does not fatigue for a lifetime  Cardiac muscle is adaptable to different organic fuels  Fatty acids (60%); glucose (35%); ketones, lactate, and amino acids (5%)  More vulnerable to oxygen deficiency than lack of a specific fuel  A cardiac conduction system: coordinates the heartbeat; consists of an internal pacemaker and nerve-like conduction pathways through myocardium  Generates and conducts rhythmic electrical signals in the following order:  The sinuatrial (SA) node: patch of modified cardiomyocytes in right atrium; serves as the pacemaker that initiates each heartbeat and determines heart rate  Signals spread throughout atria  The atrioventricular (AV) node: patch of modified cardiomyocytes serves as the electrical gateway to the ventricles; fibrous skeleton prevents signals from passing to ventricles by any other route  The atrioventricular (AV) bundle: pathway from which signals leave AV node; forks into right and left bundle branches that travel within interventricular septum  The subendocardial branches (Purkinje fibers): processes arising from lower end of bundle branches; branch extensively through ventricular myocardium  Once signals reach end of conduction system, they are perpetuated by cardiomyocytes via gap junctions Electrical and Contractile Activity of the Heart  The heart cycles through contraction and relaxation  Contraction: is called systole  Relaxation: is called diastole  These terms can refer to contraction and relaxation of either type of chamber, they usually refer to the action of the ventricles The Cardiac Rhythm  Sinus rhythm: normal heartbeat triggered by the SA node  Adult at rest is typically 70 to 80 bpm  Ectopic focus: a region of spontaneous firing other than the SA node  May govern heart rhythm if SA node is damaged  Nodal (junctional) rhythm: if SA node is damaged, heart rate is set by AV node, 40 to 50 bpm  Other ectopic foci fire at rates of 20 to 40 bpm, too slow to sustain life Pacemaker Physiology  SA node fires spontaneously at regular intervals  Mechanism:  SA node does not have a stable resting membrane potential Starts at −60 mV and drifts upward due to slow Na inflow  When it reaches threshold of −40 mV, voltage-gated Na and Ca channels open.  Faster depolarization when k channel open and k leave the cell causing repolarization  Once k channels close, pacemaker potential starts over  When SA node fires, it sets off heartbeat  As the internal pacemaker, it typically fires every 0.8 seconds, setting the resting rate at 75 bpm Electrical Behavior of the Myocardium  Action potentials of cardiomyocytes differ from those of nodal cells, neurons, muscle fibers  Cardiomyocytes have a stable resting potential of −90 mV and depolarize only when stimulated  Mechanism of cardiomyocyte action potential:  Depolarization—stimulus opens voltageregulated  Plateau—voltage-gated slow Ca channel open  Repolarization— Ca channel close and k channel open The Electrocardiogram  Detect electrical currents in heart using electrodes (leads) on skin and electrocardiograph to amplify and record the signals  Record is called an electrocardiogram (ECG or EKG)—a composite of all action potentials of nodal and myocardial cells detected  The ECG has three principal deflections:  P wave: depolarization of the atria; atrial systole begins 100 ms after start of P wave  PQ segment: time (approximately 160 ms) between P and Q deflections, represents time required for signals to pass from SA node to AV node  QRS complex: depolarization of the ventricles; ventricular systole begins shortly after  ST segment: between S and T deflections; time that ventricles are contracting Atrial repolarization also occurs, but weak signal is obscured  T wave: repolarization of the ventricles immediately prior to diastole Cardiac Arrhythmias  Deviations of ECG from normal can indicate:  Myocardial infarction (MI): abnormalities in conduction pathways, heart enlargement, and electrolyte and hormone imbalances  Ex:  Ventricular fibrillation: random electrical signals result in no pumping action; hallmark of myocardial infarction (MI) and quickly fatal  Atrial fibrillation (AF, AFib): weak rippling contraction in atria due to chaotic signals; atria fail to stimulate ventricles  Heart block: failure of part of conduction system; include bundle branch block (bundle branch failure) and total heart block (AV node failure)  Premature ventricular contraction (PVC): ventricular ectopic focus fires and sets off extra beat Blood Flow, Heart Sounds, and the Cardiac Cycle  A cardiac cycle: is one complete contraction and relaxation of all four chambers of the heart Blood pressure measured with sphygmomanometer Principles of Pressure and Flow  Events occurring on left side of heart:  When ventricle relaxes and expands, its internal pressure falls  If mitral valve is open, blood flows into left ventricle  When ventricle contracts, internal pressure rises  AV valves close, the aortic valve is pushed open and blood flows into aorta from left ventricle  Opening and closing of valves are governed by these pressure changes  AV valves limp when ventricles relaxed  Semilunar valves under pressure from blood in vessels when ventricles relaxed Valvular Insufficiency  Valvular insufficiency (incompetence): any failure of a valve to prevent reflux (regurgitation), the backward flow of blood  Valvular stenosis: cusps are stiffened and opening is constricted by scar tissue; regurgitation can be heard as a heart murmur  Mitral valve prolapse (MVP): insufficiency in which one or both mitral valve cusps bulge into atria during ventricular contraction Heart Sounds  During cardiac cycle, 2 to 3 heart sounds can be heard with a stethoscope  Auscultation: listening to sounds made by body  Heart sounds:  First heart sound S1: louder and longer “lubb,” occurs with closure of AV valves, turbulence in the bloodstream, and movements of the heart wall  Second heart sound S2: softer and sharper “dupp,” occurs with closure of semilunar valves, turbulence in the bloodstream, and movements of the heart wall  Third heart sound S3: rarely heard in people over 30; its presence may indicate enlarged or failing heart  The entire cardiac cycle: is completed in less than 1 second  Phases of the cardiac cycle:  Ventricular filling  Isovolumetric contraction  Ventricular ejection  Isovolumetric relaxation Phases of the Cardiac Cycle  Ventricular filling: Ventricles expand and their pressure drops below that of the atria  AV valves open and blood flows into the ventricles  End-diastolic volume (EDV) remains in each ventricle; about 130 mL of blood  Isovolumetric contraction:  Atria repolarize, relax and remain in diastole for rest of cardiac cycle. Ventricles depolarize, causing QRS complex, and begin to contract  AV valves close as ventricular blood surges back against the cusps. Heart sound S1 occurs at the beginning of this phase  Called isovolumetric because although ventricles contract, they do not eject blood  Pressures in aorta and pulmonary trunk are still greater than those in the ventricles  Ventricular ejection: Begins when ventricular pressure exceeds arterial pressure and semilunar valves open  rapid ejection—blood spurts out of ventricles quickly; then reduced ejection—slower flow under less pressure  T wave of ECG occurs late in this phase  Stroke volume (SV):the amount ejected—is about 70 mL  As a percentage of EDV (the ejection fraction), this is about 54%  60 mL remaining blood is end-systolic volume (ESV)  Isovolumetric relaxation:  T wave ends and ventricles begin to expand. Blood from aorta and pulmonary trunk briefly flows backward filling cusps and closing semilunar valves  Creates pressure rebound that appears as dicrotic notch in graph of artery pressure. Heart sound S2 occurs  Called isovolumetric because semilunar valves are closed and AV valves have not yet opened, so no change in blood volume  When AV valves open, ventricular filling begins again Overview of Volume Changes  Normally, right and left sides of heart eject the same volume of blood even though they are under different pressure  Congestive heart failure (CHF): results from the failure of either ventricle to eject blood effectively  Usually due to a heart weakened by myocardial infarction, chronic hypertension, valvular insufficiency, or congenital defects in heart structure Autonomic Innervation of the Heart  Heart rhythm and contraction are controlled by two cardiac centers in the medulla oblongata  Sympathetic stimulation increases heart rate and contraction strength, and dilates coronary arteries  Parasympathetic stimulation decreases heart rate Cardiac Output  The cardiac output (CO): is the amount ejected by each ventricle in 1 minute  Cardiac output (CO) = heart rate (HR) × stroke volume (SV)  CO = 75 beats/min × 70 mL/beat = 5250 mL/min Heart Rate and Chronotropic Agents  Heart rate:  measured by taking pulse (pressure surge) at point where artery runs near surface  Radial artery near wrist, common carotid artery in neck  Infant HR approximately 120 bpm or more; young adult females approximately 72 to 80 bpm; young adult males approximately 64 to 72; rises again in elderly  Variations in heart rate:  Tachycardia: persistent, resting adult HR above 100 bpm; causes by stress, anxiety, stimulants, heart disease, fever, or blood loss  Bradycardia: persistent, resting adult HR below 60 bpm; common in endurance-trained athletes, also caused by hypothermia  Positive chronotropic agents: factors that raise HR  Negative chronotropic agents: factors that lower HR Increased heart rate (HR) Positive chronotropic agents Sympathetic nervous system Epinephrine, norepinephrine Thyroid hormone Glucagon Nicotine, caffeine Hypocalcemia Increased stroke volume (SV) Increased preload (myocardial stretch) Positive inotropic agents Sympathetic nervous system Epinephrine, norepinephrine Glucagon Digitalis Nicotine, caffeine Hypercalcemia Copyright McGraw Hill LLC. 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Reduced heart rate (HR) Negative chronotropic agents Parasympathetic nervous system Acetylcholine Hypercalcemia Hypokalemia Beta blockers Increased Reduced Cardiac Output (CO = HR × SV) Reduced stroke volume (SV) Reduced preload Reduced contractility Increased afterload Negative inotropic agents Hypocalcemia Hyperkalemia Coronary Artery Disease  Coronary artery disease (CAD): degenerative disease in coronary arteries usually resulting from atherosclerosis—an accumulation of lipid deposits and necrotic tissue that obstructs the lumen and may cause a heart attack  Onset, progression, and outcomes:  Hypertension, diabetes, smoking, and other risk factors damage inner lining (endothelium) of arteries  Fatty streaks have potential to progress into lifethreatening  Alternatively, damaged vessel can scar and accumulate calcium—arteriosclerosis  Risk, prevention, and treatment:  Major risk factor is excess low-density lipoproteins (LDLs) in the blood combined with defective LDL receptors in arterial walls  Other risk factors: heredity, aging, obesity, smoking, lack of exercise, stress, hypertension, diet (especially animal fats)  Eating soluble fiber lowers blood cholesterol  CAD often treated with coronary artery bypass graft (CABG): sections of a vessel (saphenous v., small thoracic aa.) used to construct a detour around the obstruction in the coronary artery  Balloon angioplasty: another treatment for CAD; catheter threaded into coronary artery and inflated to press and flatten atheroma against arterial wall; in laser angioplasty, the atheroma is vaporized with a laser  Angioplasty less risky than CABG, but atheromas may grow back (restenosis)