PA 533 Cardiology Physiology Moodle PDF

MBKU School of PA Studies PA 533 Cardiology 2. Cardiology Physiology Medical Physiology: Chapters 17, 19, and 21-23  Objectives A. Overview of the Autonomic Nervous System 1. Compare and contrast the sympathetic and parasympathetic nervous...

MBKU School of PA Studies PA 533 Cardiology 2. Cardiology Physiology Medical Physiology: Chapters 17, 19, and 21-23  Objectives A. Overview of the Autonomic Nervous System 1. Compare and contrast the sympathetic and parasympathetic nervous systems’ influence on the cardiovascular system B. The Cardiac Cycle, The Heart as a Pump 1. Graph a cardiac cycle labeling the systole, diastole and the associated pressures 2. Relate the ECG waveforms to the mechanical events of the cardiac cycle and correlate the heart sounds 3. Describe the coordination of events leading to contraction of the heart 4. Describe the factors that contribute to and inhibit cardiac contractility C. Hemodynamics of the Cardiovascular System 1. Describe the factors used in calculating cardiac output 2. Describe the pressure, resistance and flow relationships across the cardiovascular system 3. Outline the factors that influence resistance to blood flow D. Regulation of Arterial Pressure and Cardiac Output 1. Understand the dynamics involved with regulating cardiac output 2. Locate the arterial baroreceptors and explain their influence on pressure regulation 2  Objectives E. Arteries and Veins, The Lymphatic System 1. Discuss how the velocity of blood flow is altered with the changing diameter of the vessel branches 2. Compare and contrast the pressures in the pulmonary and systemic circulation 3. Describe the factors that influence compliance of arteries and veins 4. Describe the role valves play in the movement of volume in venous and lymphatic circulation F. Microcirculation and Local Control 1. Describe the factors that influence oxygen and carbon dioxide exchange in the capillary bed 2. Identify the physical and chemical regulators of microcirculation G. Electrical Events in the Heart, The Electrocardiogram 1. Graph and define the distinct phases of the cardiac action potential 2. Follow the propagation of the electrical impulse through the heart and relate that to the ECG waveform 3  Objectives A. Overview of the Autonomic Nervous System 1. Compare and contrast the sympathetic and parasympathetic nervous systems’ influence on the cardiovascular system  ANS Control of the Cardiovascular System Parasympathetic and sympathetic innervation can modify rate, strength of contractions and vessel diameter The pacemaker sets the heart rate but can be altered Impulses from the autonomic nervous system modify the pacemaker activity  Heart rate Parasympathetic Sympathetic activity activity Autonomic control of heart rate – Parasympathetic division slows heart rate – Sympathetic division accelerates heart rate  Parasympathetic neurons release acetylcholine (ACh), slows the rate of spontaneous depolarization Sympathetic neurons release norepinephrine (NE), increases the rate of depolarization  Effects of ACh and NE on nodal and contractile cells – Acetylcholine: Stimulates muscarinic receptors Decrease heart rate Decrease force of contractions – Norepinephrine: Stimulates beta receptors Increase heart rate Increase force of contractions  Cardiac centers in the medulla oblongata – Stimulation activates sympathetic neurons Cardiac nerve Cardioacceleratory center is activated Heart rate increases – Stimulation activates parasympathetic neurons Vagus nerve Cardioinhibitory center is activated Heart rate decreases  Vagal nucleus Cardioinhibitory center Cardioacceleratory center Medulla oblongata Vagus nerve (N X) Spinal cord Sympathetic Parasympathetic Parasympathetic Sympathetic preganglionic preganglionic fiber fiber Synapses in Sympathetic ganglia cardiac plexus (cervical ganglia and Parasympathetic superior thoracic postganglionic ganglia [T1–T4]) fibers Sympathetic postganglionic fiber Cardiac nerve © 2015 Pearson Education, Inc. Heart rate: Determined by balance between inhibitory effects of vagus nerve and stimulatory effects of cardiac nerve Parasympathetic discharge is dominant under resting conditions Increasing sympathetic and decreasing parasympathetic activities increases heart rate Increasing parasympathetic and decreasing sympathetic activities decreases heart rate  Sympathetic Control of Blood Vessels – Sympathetic activation stimulates smooth muscle cells to constrict and reduce the diameter of blood vessels (vasoconstriction) – Relaxation of smooth muscle cells increases the diameter of the lumen (vasodilation)  Objectives B. The Cardiac Cycle, The Heart as a Pump 1. Graph a cardiac cycle labeling the systole, diastole and the associated pressures 2. Relate the ECG waveforms to the mechanical events of the cardiac cycle and correlate the heart sounds 3. Describe the coordination of events leading to contraction of the heart 4. Describe the factors that contribute to and inhibit cardiac contractility  The Cardiac Cycle Is the period between the start of one heartbeat and the beginning of the next Includes both contraction and relaxation Two phases 1. Systole (contraction) 2. Diastole (relaxation) Lasts about 800 msec at 75 bpm When heart rate increases, all phases of cardiac cycle shorten, particularly diastole  Blood Pressure – Rises during systole – Falls during diastole Blood flows from high to low pressure – Controlled by timing of contractions – Directed by one-way valves Phases of the Cardiac Cycle – Atrial systole – Atrial diastole – Ventricular systole – Ventricular diastole  Atrial systole begins: Atrial Start contraction forces a small amount of blood into the relaxed ventricles. Atrial systole ends; atrial diastole begins: Atrial diastole continues until the start of the next cardiac cycle. 800 0 100 msec msec msec Cardiac Ventricular systole— first phase: Ventricular cycle contraction pushes the AV valves closed but does not create enough Ventricular diastole—late: pressure to open the All chambers are relaxed. semilunar valves. The AV valves open and the ventricles fill passively. 370 msec Ventricular systole— second phase: As ventricular pressure rises and exceeds the pressure in the arteries, the semilunar valves open Ventricular diastole—early: As the and blood is ejected. ventricles relax, the ventricular blood pressure drops until reverse blood flow pushes the cusps of the semilunar valves together. Blood now flows into the relaxed atria. © 2015 Pearson Education, Inc.  ATRIAL ATRIAL ATRIAL DIASTOLE ATRIAL DIASTOLE SYSTOLE SYSTOLE VENTRICULAR VENTRICULAR VENTRICULAR DIASTOLE DIASTOLE SYSTOLE 120 5 Aortic valve closes Aortic valve opens 6 Aorta 90 Dicrotic notch 1 Atrial contraction begins. 2 Atria eject blood into ventricles. Pressure (mm Hg) 60 3 Atrial systole ends; AV valves close. Left 4 Isovolumetric ventricular contraction. 4 ventricle 7 5 Ventricular ejection occurs. 6 Semilunar valves close. Left AV 7 Isovolumetric relaxation occurs. 30 Left atrium Left AV valve closes valve opens 8 AV valves open; passive ventricular filling occurs. 2 1 3 8 0 130 End-diastolic 3 volume volume (mL) 2 ventricular 1 Left Stroke volume End-systolic volume 6 50 0 100 200 300 400 500 600 700 800 Time (msec)  Objectives B. The Cardiac Cycle, The Heart as a Pump 1. Graph a cardiac cycle labeling the systole, diastole and the associated pressures 2. Relate the ECG waveforms to the mechanical events of the cardiac cycle and correlate the heart sounds 3. Describe the coordination of events leading to contraction of the heart 4. Describe the factors that contribute to and inhibit cardiac contractility  The Electrocardiogram (ECG) Alternatively, EKG is used based on ancient Greek kardia for heart Detection of electrical activity (generated by cardiac muscle during depolarization and repolarization) reaching body surface using recording electrodes a Electrode placement for recording a standard ECG.  800 msec +1 R R P wave T wave (atria (ventricles S–T +0.5 depolarize) repolarize) P–R segment segment 0 Millivolts Q S S–T P–R interval interval Q–T QRS interval −0.5 interval (ventricles depolarize) b An ECG printout is a strip of graph paper containing a record of the electrical events monitored by the electrodes. The placement of electrodes on the body surface affects the size and shape of the waves recorded. The example is a normal ECG; the enlarged section indicates the major components of the ECG and the measurements most often taken during clinical analysis.  ONE CARDIAC CYCLE QRS QRS complex complex Electro- cardiogram T (ECG) P P ATRIAL ATRIAL ATRIAL DIASTOLE ATRIAL DIASTOLE SYSTOLE SYSTOLE VENTRICULAR VENTRICULAR VENTRICULAR DIASTOLE DIASTOLE SYSTOLE 120 5 Aortic valve closes Aortic valve opens 6 Aorta 90 Dicrotic notch 1 Atrial contraction begins. 2 Atria eject blood into ventricles. Pressure (mm Hg) 60 3 Atrial systole ends; AV valves close. Left 4 Isovolumetric ventricular contraction. 4 ventricle 7 5 Ventricular ejection occurs. 6 Semilunar valves close. Left AV 7 Isovolumetric relaxation occurs. 30 Left atrium Left AV valve closes valve opens 8 AV valves open; passive ventricular filling occurs. 2 1 3 8 0 130 End-diastolic 3 volume volume (mL) 2 ventricular 1 Left Stroke volume End-systolic volume 6 50 0 100 200 300 400 500 600 700 800 Time (msec)  120 Semilunar Semilunar valves open valves close 90 Pressure (mm Hg) 60 Left ventricle Left AV valves AV valves 30 atrium close open 0 S1 S2 S4 S3 S4 Heart sounds “Lubb” “Dupp” b The relationship between heart sounds and key events in the cardiac cycle  Objectives B. The Cardiac Cycle, The Heart as a Pump 1. Graph a cardiac cycle labeling the systole, diastole and the associated pressures 2. Relate the ECG waveforms to the mechanical events of the cardiac cycle and correlate the heart sounds 3. Describe the coordination of events leading to contraction of the heart 4. Describe the factors that contribute to and inhibit cardiac contractility  Passive filling during Atrial contraction ventricular and atrial diastole Left atrium Right atrium Right Left ventricle ventricle A B Ventricular filling Isovolumetric ventricular contraction C Ventricular ejection Isovolumetric ventricular relaxation D E Ventricular emptying  Objectives B. The Cardiac Cycle, The Heart as a Pump 1. Graph a cardiac cycle labeling the systole, diastole and the associated pressures 2. Relate the ECG waveforms to the mechanical events of the cardiac cycle and correlate the heart sounds 3. Describe the coordination of events leading to contraction of the heart 4. Describe the factors that contribute to and inhibit cardiac contractility  Cardiac Contractility measure of heart’s intrinsic contractile performance clinically used to distinguish a better performing heart from a poorly performing one enhanced contractility increases stroke volume decreasing contractility would decrease stroke volume Modifiers of contractility: ability to change [Ca2+]i positive inotropic agents: factors that increase myocardial contractility negative inotropic agents: factors that decrease myocardial contractility Positive Inotropic Agents increase [Ca2+]i Catecholamines (epinephrine, norepinephrine), cardiac glycosides (digitalis derivatives) Negative Inotropic Agents decrease [Ca2+]i Ca2+ channel blockers (such as verapamil, diltiazem and nifedipine)  Objectives C. Hemodynamics of the Cardiovascular System 1. Describe the factors used in calculating cardiac output 2. Describe the pressure, resistance and flow relationships across the cardiovascular system 3. Outline the factors that influence resistance to blood flow  Cardiac Output Cardiac Output: volume of blood pumped by each ventricle per minute Volume of blood flowing through pulmonary circulation is equivalent to volume flowing through systemic circulation  Two determinants of CO: Heart rate (beats per minute) Stroke volume (volume of blood pumped per beat) CO = heart rate X stroke volume = 70 beats per minute X 70 ml/beat = 4,900 ml/min ~ 5 liters/min  Objectives C. Hemodynamics of the Cardiovascular System 1. Describe the factors used in calculating cardiac output 2. Describe the pressure, resistance and flow relationships across the cardiovascular system 3. Outline the factors that influence resistance to blood flow  Pressure, Resistance and Flow Blood flow is driven by a constant pressure across variable resistance – Flow (F): output of the left side of heart – Pressure (P): force exerted by pumped blood on a vessel wall – Resistance (R): opposition to blood flow  Flow rate of blood is directly proportional to the pressure gradient and inversely proportional to vascular resistance F=ΔP R F is flow rate ΔP is pressure gradient: pressure difference between beginning and end of a vessel R is resistance Figure 10.2 (1) Page 345 Figure 10.2 (2) Page 345 Blood Pressure Measured as a pressure difference between two points Pressure is never expressed in absolute terms but as a pressure difference (ΔP)  ΔP between arterial and venous ends ΔP between intravascular and tissue pressure ΔP between two points at different altitudes  Pressure and flow oscillate with each heartbeat – Contraction is systole Blood is ejected into the ventricles Blood is ejected into the pulmonary trunk and the ascending aorta – Relaxation is diastole Chambers are filling with blood  Maximum systolic arterial pressure ~ 120 mm Hg, corresponds to contraction of ventricles Minimal diastolic arterial pressure ~ 80 mm Hg, corresponds to relaxation of ventricles Pulse pressure is the difference between systolic and diastolic pressures (120 - 80)  Mean arterial pressure is the main driving force producing a flow of blood It is calculated as: – mean arterial pressure = diastole pressure + 1/3 the pulse pressure Example: 80 + 1/3 (40) = 93  Objectives C. Hemodynamics of the Cardiovascular System 1. Describe the factors used in calculating cardiac output 2. Describe the pressure, resistance and flow relationships across the cardiovascular system 3. Outline the factors that influence resistance to blood flow  Resistance to Blood Flow Resistance is opposition to blood flow through a vessel It depends on three factors: blood viscosity, vessel length, and vessel radius  The major determinant to resistance to blood flow is radius of a vessel A slight change in radius produces a significant change in blood flow Blood flow in arterioles is highly affected by this relationship: – R is proportional to 1divided by the radius raised to the fourth power Figure 10.3 (2) Page 346  Objectives D. Regulation of Arterial Pressure and Cardiac Output 1. Understand the dynamics involved with regulating cardiac output 2. Locate the arterial baroreceptors and explain their influence on pressure regulation  Regulation of Cardiac Output Cardiac output depends on heart rate and stroke volume – Control of heart rate by ANS – Control of stroke volume Two types of control influence stroke volume: Intrinsic control (extent of venous return) Extrinsic control (extent of sympathetic stimulation) Both increase stroke volume by increasing strength of contraction  Stroke volume Extrinsic control Strength of cardiac contraction Intrinsic control Sympathetic activity End-diastolic volume Intrinsic control Venous return Intrinsic control: degree of diastolic filing determines cardiac muscle fiber length increase in venous return increases length of cardiac muscle fiber greater force on subsequent cardiac contraction greater stroke volume Frank-Starling law of the heart Heart pumps all blood returned to it Increased venous return results in increased stroke volume Extrinsic control (sympathetic stimulation): enhances heart contractility – increases stroke volume enhances venous return increases heart rate as well combined effect on cardiac output  Cardiac output Heart rate Stroke volume Extrinsic control Intrinsic control Parasympathetic Sympathetic End-diastolic activity activity volume Intrinsic control Venous return  Objectives D. Regulation of Arterial Pressure and Cardiac Output 1. Understand the dynamics involved with regulating cardiac output 2. Locate the arterial baroreceptors and explain their influence on pressure regulation  Baroreceptor Control of Arterial Pressure pressure sensors, baroreceptors located in carotid sinus and aortic arch part of a neural feedback mechanism regulate mean arterial pressure Carotid sinus baroreceptor Neural signals to cardiovascular control center Common carotid arteries in medulla (Blood to the brain) Aortic arch baroreceptor Aorta (Blood to rest of body)  baroreceptors (detectors) afferent neuronal pathways (to CNS) control centers (medulla) efferent neuronal pathways (from CNS) heart and blood vessels (effectors) Negative feedback loop: increased mean arterial pressure causes vasodilation and bradycardia decreased mean arterial pressure causes vasoconstriction and tachycardia  Objectives E. Arteries and Veins, The Lymphatic System 1. Discuss how the velocity of blood flow is altered with the changing diameter of the vessel branches 2. Compare and contrast the pressures in the pulmonary and systemic circulation 3. Describe the factors that influence compliance of arteries and veins 4. Describe the role valves play in the movement of volume in venous and lymphatic circulation  The Vascular Tree The vascular tree consists of arteries, arterioles, capillaries, venules and veins arteries as a distribution system microcirculation as a diffusion and filtration system veins as a collection system  Physical properties of vessels closely follow the level of branching in the circuit: – The aorta branches out into billions of capillaries that ultimately regroup into a single vena cava – At each level of arborization of peripheral circulation, values of several key parameters vary dramatically  Airway Lungs Pulmonary Air sac capillaries Arterioles Venules Pulmonary Pulmonary Pulmonary artery circulation veins Aorta (major Systemic systemic veins artery) Systemic circulation Systemic Smaller arteries capillaries branching off to supply Venules Arterioles various tissues For simplicity, only two capillary beds within two Tissues organs are illustrated. Key Parameters: Number, radius, cross-sectional area of vessels Velocity of blood flow and blood volume Pressure Structure and elastic properties of vascular walls Number of vessels increases enormously from a single aorta to small arteries, arterioles, and finally capillaries Radius of an individual vessel declines as a result of arborization, decreasing from 1.1 cm in the aorta to ∼3 μm in the smallest capillaries Cross-sectional area proportional to square of the radius decreases even more precipitously aggregate cross-sectional area is sum of single cross- sectional areas of all parallel vessels at that level of branching Fundamental law of vessel branching at each branch point, combined cross- sectional area of daughter vessels exceeds cross-sectional area of parent vessel steepest increase in total cross-sectional area occurs in microcirculation Mean linear velocity of flow is inversely related to total cross-sectional area must be minimal in capillaries where cross- sectional area is maximal is maximal in the aorta is less in vena cava, with a cross-sectional area ∼50% larger than aorta  Objectives E. Arteries and Veins, The Lymphatic System 1. Discuss how the velocity of blood flow is altered with the changing diameter of the vessel branches 2. Compare and contrast the pressures in the pulmonary and systemic circulation 3. Describe the factors that influence compliance of arteries and veins 4. Describe the role valves play in the movement of volume in venous and lymphatic circulation  Pressures in Pulmonary and Systemic Circulations intravascular pressures in systemic circuit are higher than pulmonary circuit total resistance of systemic circulation is far higher than pulmonary circulation  upstream driving pressure ∼95 mm Hg in systemic circulation but only ∼15 mm Hg in pulmonary circulation circulation can be divided into a high- pressure and a low-pressure system  high-pressure system extends from left ventricle in the contracted state all the way to systemic arterioles low-pressure system extends from systemic capillaries into right side of heart and then through pulmonary circuit into left side of heart in the relaxed state pulmonary circuit is a low-pressure system; mean arterial pressures do not exceed 15 mm Hg  Objectives E. Arteries and Veins, The Lymphatic System 1. Discuss how the velocity of blood flow is altered with the changing diameter of the vessel branches 2. Compare and contrast the pressures in the pulmonary and systemic circulation 3. Describe the factors that influence compliance of arteries and veins 4. Describe the role valves play in the movement of volume in venous and lymphatic circulation  Compliance of Arteries and Veins Compliance of vessel walls Is how easily they can be stretched Depends on volume and pressure of blood contained within the vessel Is expressed as change in volume over change in pressure  Arteries have a low volume capacity but can withstand large transmural pressure differences Veins have a large volume capacity but can withstand only small transmural pressure differences  compliance of arteries decreases only modestly with further increases in pressure compliance of veins is far higher than for arteries in low-pressure range but quite low at higher pressures  Objectives E. Arteries and Veins, The Lymphatic System 1. Discuss how the velocity of blood flow is altered with the changing diameter of the vessel branches 2. Compare and contrast the pressures in the pulmonary and systemic circulation 3. Describe the factors that influence compliance of arteries and veins 4. Describe the role valves play in the movement of volume in venous and lymphatic circulation  Role of Valves in Fluid Movement Large veins are equipped with one-way valves spaced at 2 to 4 cm intervals Valves permit blood to move forward toward the heart and prevent it from moving back into tissues Venous valves counteract the effect of gravity on venous return Closure of valves inside veins ensures that blood does not flow backward Vein Open venous valve permits flow of blood toward heart Contracted skeletal muscle Closed venous valve prevents backflow of blood  The lymphatic system is an accessory route for return of interstitial fluid to blood one-way vessels that begins with initial lymphatics, small blind-ended terminal lymph vessels Endothelial cells of initial lymphatics slightly overlap This arrangement creates one-way, valve-like openings in vessel wall Fluid pressure outside opens these valves, permitting interstitial fluid to enter  Lymph is interstitial fluid that enters a lymphatic vessel Fluid pressure inside forces overlapping edges together, closing the valve Valve-like openings are large enough to allow entry of escaped plasma proteins and bacteria To venous system Arteriole Interstitial fluid Tissue cells Venule Blood capillary Initial lymphatic  Fluid pressure on the outside of the vessel pushes the endothelial cell’s free edge inward, permitting entrance of interstitial fluid (now lymph). Overlapping endothelial cell Interstitial fluid Lymph Fluid pressure on the inside of the vessel forces the overlapping edges together so that lymph cannot escape.  Objectives F. Microcirculation and Local Control 1. Describe the factors that influence oxygen and carbon dioxide exchange in the capillary bed 2. Identify the physical and chemical regulators of microcirculation Gas Exchange in the Capillary Bed Capillaries are the sites of exchange between blood and body cells Exchange is accomplished by diffusion Diffusion is enhanced by minimizing distance and maximizing surface area – Capillary thin walls and extensive branching – Capillary abundance  Capillary walls are very thin: one single layer of flat endothelial cells Each capillary is very narrow that plasma contents are in direct contact or within diffusing distance from capillary wall Tissue cells are very close to capillaries  Capillaries are very abundant, offering a large surface area to serve cells Blood flow is slow in capillaries due to extensive branching Tremendous cross-sectional area of all capillaries in an area enhances diffusion  Objectives F. Microcirculation and Local Control 1. Describe the factors that influence oxygen and carbon dioxide exchange in the capillary bed 2. Identify the physical and chemical regulators of microcirculation  Regulation of Microcirculation Vascular smooth muscle cells (VSMCs) have spontaneous rhythmic variations in tension – leads to periodic changes in vascular resistance and microcirculatory flow – Active contraction of VSMCs regulates resistance upstream of capillary bed to adjust perfusion VSMCs receive multiple excitatory as well as inhibitory inputs – Inputs come from chemical synapses and circulating chemicals  various membrane proteins (channels, transporters, and receptors) control the tone of VSMCs these membrane proteins lead to either contraction (vasoconstriction) or relaxation (vasodilation) Normal arteriolar tone Cross section of arteriole Vasoconstriction (increased contraction of circular smooth muscle in the arteriolar Caused by: wall, which leads to Myogenic activity increased resistance Oxygen (O2) and decreased Carbon dioxide (CO2) flow through the vessel) and other metabolites Endothelin Sympathetic stimulation Vasopressin; angiotensin II Cold Vasodilation (decreased contraction of circular smooth muscle in the arteriolar Caused by: wall, which leads to Myogenic activity decreased resistance Oxygen (O2) and increased flow Carbon dioxide (CO2) through the vessel) and other metabolites Nitric oxide Sympathetic stimulation Histamine release Heat  Objectives G. Electrical Events in the Heart, The Electrocardiogram 1. Graph and define the distinct phases of the cardiac action potential 2. Follow the propagation of the electrical impulse through the heart and relate that to the ECG waveform  Cardiac Action Potentials Pacemaker activity of cardiac autorhythmic cells: SA node, AV node and bundle of His Action potential of contractile cardiac muscle cells: atrial and ventricular muscle cells Pacemaker potential: Initial phase of slow depolarization to threshold Rising phase once threshold is reached Falling phase of repolarization  Self-induced action potential Threshold potential Slow depolarization (pacemaker potential) Action potential in autorhythmic cells: slow depolarization to threshold rising phase falling phase of repolarization Plateau phase of action potential Threshold potential Action potential in cardiac contractile cells: Cells at rest until excited Rapid rising phase to + membrane potential value Plateau phase in + membrane potential Rapid falling phase of repolarization  Fast and Slow Responses in Heart Tissue Autorhythmic cells have different rates of: depolarization to threshold action potential discharge Tissue Action Potential Per Minutes SA node 80-100 AV node 40-60 Bundle of His and 20-40 Purkinje fibers Cell A Threshold potential Faster rate of depolarization Cell B Threshold potential Slower rate of depolarization  Objectives G. Electrical Events in the Heart, The Electrocardiogram 1. Graph and define the distinct phases of the cardiac action potential 2. Follow the propagation of the electrical impulse through the heart and relate that to the ECG waveform Electrical Activity of the Hearth Pacemaker activity: 1. cardiac action potential originates in the sinoatrial (SA) node – located in the right atrium – cells depolarize spontaneously and fire off action potentials at a regular, intrinsic rate between 80 and 100 times per minute – cell activity affected by ANS  Interatrial pathway Atrioventricular Sinoatrial (AV) node (SA) node Right Left atrium atrium Internodal Left pathway branch of bundle of His Right Left branch ventricle of bundle of His Right ventricle Purkinje fibers 2. spontaneous action potential conducts from cell to cell throughout right atrial muscle and spread to left atrium via – gap junctions – interatrial pathway: from SA node to LA – both atria depolarize to contract simultaneously 3. signal arrives at atrioventricular (AV) node – internodal pathway: from SA to AV node – sequential contraction of ventricles – AV nodal delay: conduction of action potential through AV node is slow; impulse delayed 100 msec 4. impulse travel from AV node to His- Purkinje fiber system, carries signal to muscle of both ventricles – coordinates spread of ventricular excitation to ensure ventricles contract as a unit  Interatrial pathway Right atrium Left atrium SA node AV node Internodal pathway Purkinje fibers Bundle of His Right ventricle Left ventricle Movement of Electrical Impulses through the Conducting System 1 2 3 4 5 Time = 0 Elapsed time = 50 msec Elapsed time = 150 msec Elapsed time = 175 msec Elapsed time = 225 msec AV bundle Bundle Moderator Purkinje SA node AV node band branches fibers The SA node depolar- Depolarization spreads Atrial contraction begins. Impulses travel along the The impulse is distributed izes and atrial activa- across the atrial surfaces The AV node delays the AV bundle within the interven- by Purkinje fibers and tion begins. and reaches the AV node. spread of electrical tricular septum to the apex of relayed throughout the activity to the AV bundle the heart. Impulses also ventricular myocardium. by 100 msecs. spread to the papillary Atrial contraction is muscles of the right ventricle completed and ventricular by the moderator band. contraction begins. © 2015 Pearson Education, Inc.  800 msec +1 R R P wave T wave (atria (ventricles S–T +0.5 depolarize) repolarize) P–R segment segment 0 Millivolts Q S S–T P–R interval interval Q–T QRS interval −0.5 interval (ventricles depolarize) b An ECG printout is a strip of graph paper containing a record of the electrical events monitored by the electrodes. The placement of electrodes on the body surface affects the size and shape of the waves recorded. The example is a normal ECG; the enlarged section indicates the major components of the ECG and the measurements most often taken during clinical analysis.