Copyright © 2004 Pearson Education, Inc., publishing as Benjamin Cummings Cardiac Physiology Keri Muma Bio 6

Copyright © 2004 Pearson Education, Inc., publishing as Benjamin Cummings The Cardiovascular System  Cardiovascular system is composed of:  The heart and blood vessels  Functions in transportation of blood:  delivers oxygen and nutrients to tissues  removes carbon dioxide and waste products from tissues

Copyright © 2004 Pearson Education, Inc., publishing as Benjamin Cummings Gross Anatomy of the Heart

Copyright © 2004 Pearson Education, Inc., publishing as Benjamin Cummings Microscopic Anatomy of Heart Muscle  Cardiac muscle is striated, short, fat, branched, and interconnected  Intercalated discs anchor cardiac cells together and allow free passage of ions through gap junction

Copyright © 2004 Pearson Education, Inc., publishing as Benjamin Cummings The heart  Myocardial cells:  99% of the heart is made of contractile cardiac muscle cells  Generates the force of contraction produced by the heart  1% is autorhythmic cells that are self-excitable  Generate action potentials spontaneously without neural stimuli

Copyright © 2004 Pearson Education, Inc., publishing as Benjamin Cummings Intrinsic Conduction System  Autorhythmic cells composed the intrinsic conduction system of the heart  Coordinates the rhythmic excitation and contraction of the cardiac muscle to ensure efficient pumping

Copyright © 2004 Pearson Education, Inc., publishing as Benjamin Cummings Intrinsic Conduction System  The action potential generated by autorhythmic cells travel through the conduction system and to surrounding myocardial tissue by gap junction

Copyright © 2004 Pearson Education, Inc., publishing as Benjamin Cummings Intrinsic Conduction System  Sequence of Excitation  Sinoatrial (SA) node –pacemaker, generates impulse (70 times/minute)  Atrioventricular (AV) node (40-60 times/minute), delays the impulse about 0.1 second  Impulse passes from atria to ventricles via the atrioventricular bundle (bundle of His)

Copyright © 2004 Pearson Education, Inc., publishing as Benjamin Cummings Intrinsic Conduction System  AV bundle splits into two pathways in the interventricular septum (bundle branches)  Bundle branches carry the impulse toward the apex of the heart (35 times/minute)  Purkinje fibers carry the impulse from the heart apex to the ventricular walls (30 times/minute)

Copyright © 2004 Pearson Education, Inc., publishing as Benjamin Cummings Intrinsic Conduction System  Ectopic focus – abnormal overly excitable area begins to depolarizes faster than the SA node  Can lead to a premature heartbeat (extrasystole) and/or accelerated heart rate  Can be caused by heart disease, anxiety, lack of sleep, to much caffeine, nicotine

Copyright © 2004 Pearson Education, Inc., publishing as Benjamin Cummings Heart Physiology: Intrinsic Conduction System  What gives autorhythmic cells the unique ability to spontaneously generate action potentials?  They have an unstable membrane potentials called pacemaker potentials  Their membrane gradually depolarizes and drifts towards threshold due to slow Na+ entry  When threshold is reached they fire an action potential  Calcium influx (rather than sodium) causes the depolarization phase of the action potential  Repolarization is cause by K+ efflux

Copyright © 2004 Pearson Education, Inc., publishing as Benjamin Cummings Pacemaker and Action Potentials of the Heart Figure 18.13

Copyright © 2004 Pearson Education, Inc., publishing as Benjamin Cummings Electrocardiography  EKG – tracing of the electrical currents created by the intrinsic conduction system  Test to screen for a variety of cardiac abnormalities

Copyright © 2004 Pearson Education, Inc., publishing as Benjamin Cummings Electrocardiography  P wave – atrial depolarization  QRS complex – ventricles depolarization  T wave – ventricles repolarization

Copyright © 2004 Pearson Education, Inc., publishing as Benjamin Cummings Cardiac Abnormalities  Bradycardia - <60 BPM  Tachycardia - >100 BPM  Arrhythmias – uncoordinated atrial and ventricular contractions  Damaged SA node – pace set by AV node ~ 50 BPM  Heart block – damage to the AV node, ventricles contract at ~30 BPM  Fibrillation – irregular chaotic twitching of the myocardium

Copyright © 2004 Pearson Education, Inc., publishing as Benjamin Cummings

Cardiac Abnormalities

Copyright © 2004 Pearson Education, Inc., publishing as Benjamin Cummings Cardiac Muscle Contraction  Contraction of cardiac muscle cells:  Must be stimulated by autorhythmic cells to contract  Have a long absolute refractory period  Prevents summation and tetany  Ensures filling of the chambers

Copyright © 2004 Pearson Education, Inc., publishing as Benjamin Cummings Action potentials in Cardiac Muscle Cells  Contractile myocardial cells have a stable resting membrane potential  Depolarization wave travels through the gap junctions and opens fast voltage gated Na+ channels in the contractile cell  Triggers an action potential  Na+ channels close and slow Ca2+ channels open causing Ca2+ influx from the ECF  Plateau phase – Ca2+ influx prolongs the action potential and prevents rapid repolarization  Ca2+ close and K+ channels open causing repolarization

Copyright © 2004 Pearson Education, Inc., publishing as Benjamin Cummings Comparison of Action Potentials

Copyright © 2004 Pearson Education, Inc., publishing as Benjamin Cummings Contraction of Cardiac Muscle  Cardiac muscle contraction is similar to skeletal muscle contraction  The action potential traveling down the T- tubules triggers the influx of Ca2+ from the ECF  The Ca2+ influx induces the release of additional Ca2+ from the SR  Ca2+ binds to troponin allowing sliding of the myofilaments

Copyright © 2004 Pearson Education, Inc., publishing as Benjamin Cummings Metabolism of Cardiac Muscle  Relies almost exclusively on aerobic respiration  Constant and adequate blood supply is critical  Adaptive to multiple fuel sources: glucose, fatty acids, lactic acid)

Copyright © 2004 Pearson Education, Inc., publishing as Benjamin Cummings Cardiac Cycle  Contraction of the myocardium must occur in a coordinated rhythm to ensure proper pumping of blood  Atrial excitation and contraction must be completed before ventricular contraction occurs  Cardiac cycle refers to all events associated with one complete heart beat  Systole – contraction of heart muscle  Diastole – relaxation of heart muscle

Copyright © 2004 Pearson Education, Inc., publishing as Benjamin Cummings Phases of the Cardiac Cycle  Ventricular filling - Mid-to-late diastole  Blood passively flows into ventricles from atria  Atria contract (atrial systole)  AV valves open, SL valves closed

Copyright © 2004 Pearson Education, Inc., publishing as Benjamin Cummings Phases of the Cardiac Cycle  Ventricular systole  Atrial diastole  Rising ventricular pressure results in closing of AV valves  Isovolumetric contraction phase  Ventricular ejection phase opens semilunar valves

Copyright © 2004 Pearson Education, Inc., publishing as Benjamin Cummings Phases of the Cardiac Cycle  Isovolumetric relaxation – early diastole  Ventricles relax  Backflow of blood in aorta and pulmonary trunk closes semilunar valves  Atria re-filling  Atria pressure increases, AV valves open and cycle repeats

Copyright © 2004 Pearson Education, Inc., publishing as Benjamin Cummings Heart Sounds  Heart sounds (lub-dup) are associated with closing of heart valves  First sound occurs as AV valves close and signifies beginning of systole  Second sound occurs when SL valves close at the beginning of ventricular diastole

Copyright © 2004 Pearson Education, Inc., publishing as Benjamin Cummings Operation of AV Valves

Copyright © 2004 Pearson Education, Inc., publishing as Benjamin Cummings Operation of SL Valves

Copyright © 2004 Pearson Education, Inc., publishing as Benjamin Cummings Summary: Figure 18.20

Copyright © 2004 Pearson Education, Inc., publishing as Benjamin Cummings Cardiac Output (CO) and Reserve  Cardiac Output - the amount of blood pumped by each ventricle in one minute  CO = (heart rate [HR]) x (stroke volume [SV])  HR is the number of heart beats per minute  SV is the amount of blood pumped out by a ventricle with each beat  Cardiac reserve is the difference between resting and maximal CO

Copyright © 2004 Pearson Education, Inc., publishing as Benjamin Cummings Cardiac Output: Example  CO (ml/min) = HR (75 beats/min) x SV (70 ml/beat)  CO = 5250 ml/min (5.25 L/min)

Copyright © 2004 Pearson Education, Inc., publishing as Benjamin Cummings Regulation of Heart Rate  Heart rate is modulated by the autonomic nervous system  Parasympathetic activity – slows HR down via ACh  Increases K+ permeability, hyperpolarization  Sympathetic activity–increases HR via NE/E  Increases Na+, and Ca2+ channels, speeds up depolarization

Copyright © 2004 Pearson Education, Inc., publishing as Benjamin Cummings Regulation of Heart Rate  Chronotropic agents – affect heart rate  Positive chronotropic factors increase heart rate  Negative chronotropic factors decrease heart rate

Copyright © 2004 Pearson Education, Inc., publishing as Benjamin Cummings Regulation of Heart Rate  Hormones  Epinephrine and Thyroxine increase HR  Ions  Elevated K+ and Na+ levels in the ECF– decrease HR  Elevated Ca2+ levels in the ECF – increases HR  Physical factors  Age – decreases HR  Exercise – increases HR  Temperature – increases HR

Copyright © 2004 Pearson Education, Inc., publishing as Benjamin Cummings Regulation of Stroke Volume  Stroke volume = end diastolic volume (EDV) minus end systolic volume (ESV)  EDV = amount of blood collected in a ventricle during diastole  ESV = amount of blood remaining in a ventricle after contraction  Ejection factor = SV/EDV

Copyright © 2004 Pearson Education, Inc., publishing as Benjamin Cummings Factors Affecting Stroke Volume  Preload – amount ventricles are stretched by contained blood, dependent on EDV  Frank-Starling’s Law: increased stretch = increased contraction strength  Affected by volume of venous return and ventricular filling time  Factors that would increase preload:  Exercise  Slower heart beat  Factors that would decrease preload  Blood loss  Rapid heart beat

Copyright © 2004 Pearson Education, Inc., publishing as Benjamin Cummings Factors Affecting Stroke Volume  After load – back pressure exerted by blood in the large arteries leaving the heart  Increase in after load decreases stroke volume  Atherosclerosis, arteriostenosis, hypertension, loss of elasticity of blood vessels

Copyright © 2004 Pearson Education, Inc., publishing as Benjamin Cummings Extrinsic Factors Influencing Stroke Volume  Contractility – cardiac cell contractile force due to factors independent of stretch and EDV  Inotropic agents – effect contractility  Increase in contractility comes from:  Increased sympathetic stimuli  Hormones – thyroxine, epinephrine  Increased ECF Ca 2+ and some drugs like digitalis

Copyright © 2004 Pearson Education, Inc., publishing as Benjamin Cummings Contractility and Norepinephrine  Sympathetic stimulation releases norepinephrine and initiates a cyclic AMP second- messenger system Figure 18.22

Copyright © 2004 Pearson Education, Inc., publishing as Benjamin Cummings Extrinsic Factors Influencing Stroke Volume  Agents/factors that decrease contractility include:  Acidosis  Increased extracellular Na+ and K +  Calcium channel blockers

Copyright © 2004 Pearson Education, Inc., publishing as Benjamin Cummings Factors Affecting Cardiac Output

Copyright © 2004 Pearson Education, Inc., publishing as Benjamin Cummings Factors Involved in Regulation of Cardiac Output Figure 18.23