Chapter 19: The Circulatory System: The Heart

Chapter 19: The Circulatory System: The Heart
Co 19 Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display. Chapter 19: The Circulatory System: The Heart Gondelon/Photo Researchers, Inc.

Circulatory System Circulatory system Blood Heart Vessels
Cardiovascular system 19-3

Circulatory System: The Heart
Overview of Cardiovascular System Gross Anatomy of the Heart Cardiac Conduction System and Cardiac Muscle Electrical and Contractile Activity of Heart Blood Flow, Heart Sounds, and Cardiac Cycle Cardiac Output 19-2

Cardiology – the scientific study of the heart and the treatment of its disorders For Information on the field of Cardiology visit: htm

Two Major Circuits of the Circulatory System Pulmonary Circuit Systemic Circuit Pulmonary Circuit occupies the Right Side of Heart Systemic Circuit occupies the Left Side of the Heart

Two Major divisions of Circulatory System Pulmonary Circuit Pumps blood through the Lungs Carries blood to lungs for gas exchange and back to heart Right side of heart Systemic Circuit Pump blood through the Body Supplies oxygenated blood to all tissues of the body and returns it to the heart Left side of heart

Fig. 19.1 CO2 O2 Pulmonary circuit O2-poor, CO2-rich blood O2-rich,
Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display. CO2 O2 Pulmonary circuit O2-poor, CO2-rich blood O2-rich, CO2-poor blood Systemic circuit CO2 O2

Cardiovascular System Circuit
Pulmonary Circuit First, low O2 blood from the body enters heart Second, heart pumps blood to the lungs Systemic Circuit First, high O2 blood from lungs returns to heart Second, heart pumps blood to all body systems Veins carry blood to the heart Arteries carry blood from the heart

High O2 blood from lungs returns to heart
Fig. 19.1 Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display. CO2 O2 High O2 blood from lungs returns to heart Heart pumps blood to the lungs Pulmonary circuit O2-poor, CO2-rich blood O2-rich, CO2-poor blood Systemic circuit Low O2 blood from the body enters heart Heart pumps blood to all body systems CO2 O2

Pulmonary Circuit Right side of Heart Low O2 blood enters heart via inferior and superior vena cava Blood leaves heart to lungs via pulmonary trunk (arteries) Systemic Circuit Left side of Heart High O2 blood from lungs enters heart via pulmonary veins Blood sent to all organs of the body via aorta Veins carry blood to the heart Arteries carry blood from the heart

High O2 blood from lungs enters heart via pulmonary veins
Fig. 19.1 Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display. CO2 O2 High O2 blood from lungs enters heart via pulmonary veins Blood leaves heart to lungs via pulmonary trunk (arteries) Pulmonary circuit O2-poor, CO2-rich blood O2-rich, CO2-poor blood Systemic circuit Low O2 blood enters heart via inferior and superior vena cava Blood sent to all organs of the body via aorta CO2 O2

Pulmonary Circuit Right side of Heart Inferior and Superior Vena Cava return blood to the Right Atrium of the heart The Right Ventricle pumps blood to lungs via Pulmonary Trunk (arteries) Systemic Circuit Left side of Heart High O2 blood from the pulmonary veins enters the Left Atrium of the heart The Left Ventricle of the heart pumps blood to the body via Aorta Blood enters the heart through the Atria Blood leaves the heart through the Ventricles

The Left Ventricle of the heart pumps blood to the body via Aorta
Fig. 19.1 Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display. CO2 O2 The Right Ventricle pumps blood to lungs via Pulmonary Trunk (arteries) High O2 blood from the pulmonary veins enters the Left Atrium of the heart Pulmonary circuit O2-poor, CO2-rich blood O2-rich, CO2-poor blood Systemic circuit Inferior and Superior Vena Cava return blood to the Right Atrium of the heart The Left Ventricle of the heart pumps blood to the body via Aorta CO2 O2

Systemic Circuit Pulmonary Circuit Uses Left side of
Fig. 19.1 Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display. CO2 O2 Systemic Circuit Uses Left side of Heart Blood enters SC through the Left Atrium Blood leaves SC Ventricle Pulmonary Circuit Uses Right side of Heart Blood enters PC through the Right Atrium Blood leaves PC through the Right Ventricle Pulmonary circuit O2-poor, CO2-rich blood O2-rich, CO2-poor blood Systemic circuit CO2 O2

Veins carry blood to the heart Arteries carry blood from the heart and Blood enters the heart through the Atria Blood leaves the heart through the Ventricles Therefore, Veins return blood to the Atria Arteries carry blood from the Ventricles

Cardiovascular System Circuit: Unity of Form and Function
Atrium are Superior Ventricles are Inferior The Atria are thinned walled, little muscle The Ventricles are thick walled, very muscular The Left Ventricle is much larger than the right Ventricle

Position, Size, and Shape
Heart located in Mediastinum Tilts to the left Base wide, superior portion of heart Apex inferior end tapers to point Approximately size of fist Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display. Aorta Pulmonary trunk Superior vena cava Right lung Base of heart Parietal pleura (cut) Pericardial sac (cut) Apex of heart Diaphragm (c) Figure 19.2c 19-5

Fig. 19.2c Aorta Pulmonary trunk Superior vena cava Base of Right lung
Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display. Aorta Pulmonary trunk Superior vena cava Base of heart Right lung Parietal pleura (cut) Pericardial sac (cut) Apex of heart Diaphragm (c)

Sternum 3rd rib Diaphragm (a) Fig. 19.2a
Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display. Sternum 3rd rib Diaphragm (a)

Pericardial Cavity Body cavity containing the heart
Lined by the Pericardium Anchored to diaphragm inferiorly and sternum anteriorly Filled with mL of Pericardial Fluid Functions: Allows heart to beat without friction, Provides room to expand Resists excessive expansion

Posterior Lungs Thoracic vertebra Pericardial cavity Left ventricle
Fig. 19.2b Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display. Posterior Lungs Thoracic vertebra Pericardial cavity Left ventricle Right ventricle Interventricular septum Sternum (b) Anterior

Pericardium Pericardium Structure:
Double-walled membrane sac (pericardial sac) that encloses the heart Parietal Pericardium Outer wall of pericardial sac; lines pericardial cavity Superficial fibrous layer of connective tissue Serous membrane layer - recall: serous membranes line body cavities that do not open to the outside Visceral Pericardium (Epicardium) Inner wall of pericardial cavity; covers the heart Serous lining of sac turns inward at base of heart to cover the heart surface 19-7

Pericardium and Heart Wall
Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display. Pericardial cavity Pericardial sac: Fibrous layer Serous layer Epicardium Myocardium Endocardium Epicardium Pericardial sac Figure 19.3 19-8

Pericardial cavity sac: Fibrous layer Serous layer Epicardium
Fig. 19.3b Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display. Pericardial cavity sac: Fibrous layer Serous layer Epicardium

Heart Wall Epicardium Superficial Myocardium Endocardium Deep
The Heart Wall is Composed of 3 Tissue Layers: Epicardium Superficial Myocardium Endocardium Deep

Heart Wall Epicardium The Visceral Pericardium
Serous membrane covering heart Adipose in thick layer in some places Coronary Blood Vessels travel through this layer Supply the heart tissue with blood 19-10

Heart Wall Myocardium Layer of cardiac muscle
Fibrous skeleton of the heart framework of collagenous and elastic fibers provides structural support and attachment for cardiac muscle and anchor for valve tissue electrical insulation between atria and ventricles important in timing and coordination of contractile activity

Fig. 19.6 Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display. (a) (b) Photo and illustration by Roy Schneider, University of Toledo. Plastinated heart model for illustration courtesy of Dr. Carlos Baptista, University of Toledo

Heart Wall Endocardium Smooth inner lining of heart and blood vessels
Covers the valve surfaces Continuous with endothelium of blood vessels

© The McGraw-Hill Companies, Inc.
Fig. 19.4a Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display. Epicardium: Fat in interventricular sulcus Left ventricle Right ventricle Anterior interventricular artery (a) Anterior view, external anatomy © The McGraw-Hill Companies, Inc.

© The McGraw-Hill Companies, Inc.
Fig. 19.4b Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display. Superior vena cava Base of heart Inferior vena cava Right atrium Interatrial septum Left atrium Opening of coronary sinus Right AV valve Left AV valve Trabeculae carneae Coronary blood vessels Right ventricle Tendinous cords Papillary muscles Left ventricle Endocardium Epicardial fat Myocardium Interventricular septum Epicardium Apex of heart (b) Posterior view, internal anatomy © The McGraw-Hill Companies, Inc.

2. Gross Anatomy of the Heart
External Structure Internal Structure

Is this an Anterior or Posterior view of the Heart?
Fig. 19.6a Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display.

A. External Anatomy - Anterior
Aortic arch Ascending aorta Superior vena cava Left pulmonary artery Branches of the right pulmonary artery Pulmonary trunk Left pulmonary veins Right pulmonary veins Left auricle of Left Atrium Right auricle Right atrium Right ventricle Inferior vena cava Left ventricle Apex of heart Fig. 19.5a (a) Anterior view Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display.

B. External Anatomy -Posterior
Aorta Left pulmonary artery Superior vena cava Right pulmonary artery Left pulmonary veins Right pulmonary veins Left atrium Right atrium Inferior vena cava Fat Left ventricle Apex of heart Right ventricle (b) Posterior view Fig. 19.5b Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display.

Structure of Cardiac Muscle
Cardiocytes Cells of the heart Form the Myocardium, compose the heart walls A type of muscle cell Striated Involuntary Repair of damage of cardiac muscle is almost entirely by fibrosis (scarring) 19-28

Structure of Cardiac Muscle: Cardiocytes
Histological Differentiation Striated Branched Cells Contain Glycogen Intercalated Disks

Striations Nucleus Intercalated discs (a) Fig. 19.11a
Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display. Striations Nucleus Intercalated discs (a) © Ed Reschke

Striated myofibril Glycogen Nucleus Mitochondria Intercalated discs
Fig b Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display. Striated myofibril Glycogen Nucleus Mitochondria Intercalated discs (b)

Intercalated Disks Tightly join cardiocytes end to end Interdigitating Folds – cell membrane folds interlock with each other, and increase surface area of contact Mechanical Cell-to-Cell Junctions Fascia Adherens – broad band of protein anchors the actin of the thin myofilaments to the plasma membrane Desmosomes - weldlike mechanical junctions between cells

Intercalated Disks Tightly join cardiocytes end to end Gap Junctions - specialized cell-to-cell junctions that allow ion to flow between cells Electrical Junctions – adjacent cells can stimulate neighbors entire myocardium of either two atria or two ventricles acts like single unified cell crucial for synchronized heart beat

Intercellular space Desmosomes Gap junctions (c) Fig. 19.11c
Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display. Intercellular space Desmosomes Gap junctions (c)

Metabolism of Cardiac Muscle
Cardiac Muscle depends almost exclusively on Aerobic Respiration to make ATP Cardiocytes: Rich in Myoglobin - a specialized form of hemoglobin Rich in Glycogen - the fuel for Aerobic Respiration Highly Developed Mitochondria - The organelle for Cellular Respiration fill 25% of cell 19-30

Metabolism of Cardiac Muscle
Cardiac Muscle Adaptable to Organic Fuels fatty acids (60%), glucose (35%), ketones, lactic acid and amino acids (5%) Fatigue Resistant makes little use of anaerobic fermentation or oxygen debt mechanisms avoids producing bi-products of anaerobic respiration like lactic acid does not fatigue for a lifetime More vulnerable to oxygen deficiency than lack of a specific fuel 19-30

Cardiac Conduction System: Coordination of the Heart Beat
System of specialized cells, innervations, and cell junctions working together to coordinate the heart beat Very important processes for an efficient heart beat Main Components of system include: an Internal Pacemaker of specialized cardiocytes Nervelike Conduction Pathways through myocardium Work together to generate and conduct rhythmic electrical signals through the myocardium 19-31

Cardiac Conduction System
Internal Pacemaker of specialized cardiocytes: Sinoatrial (SA) Node Group of modified cardiocytes known as the Pacemaker Located in right atrium near base of Superior Vena Cava Initiates each heartbeat and determines heart rate signals spread throughout atria 19-31

Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display. 1 SA node fires. 2 Excitation spreads through atrial myocardium. Right atrium 1 2 Sinoatrial node (pacemaker) Left atrium 3 AV node fires. 2 Purkinje fibers Atrioventricular node 3 4 Excitation spreads down AV bundle. Bundle branches Atrioventricular bundle 5 Purkinje fibers distribute excitation through ventricular myocardium. 4 5 Purkinje fibers Figure 19.12 19-32

Internal Pacemaker of specialized cardiocytes: Atrioventricular (AV) Node Specialized cardiocytes located near the right AV valve at lower end of interatrial septum Propagate electrical signal to the ventricles Fibrous skeleton acts as an insulator to prevent currents from getting to the ventricles from any other route Atrioventricular (AV) Bundle (bundle of His) Bundle of conducting tissue that travels from AV node through interventricular septum Bundle branches into RV and LV at apex 19-31

Internal Pacemaker of specialized cardiocytes: Purkinje Fibers Nervelike processes that spread from Bundle of His and distribute throughout ventricular myocardium Distribute excitation through ventricular myocardium Conduct signal from cell to cell through gap junctions 19-31

Nerve Supply to Heart The heart also receives sympathetic and parasympathetic innervation Important for adaptation and modification of cardiac output modifies heart rate modifies heart contractility (contraction strength)

Nerve Supply to Heart Sympathetics Sympathetic stimulation:
Raises heart rate Increases contractility Increases Cardiac Output Dilates coronary arteries Sympathetic Innervation: Sympathetic pathway to the heart originates in the lower cervical to upper thoracic segments of the spinal cord Continues to adjacent sympathetic chain ganglia Some pass through cardiac plexus in mediastinum Continue as cardiac nerves to the heart Fibers terminate in SA and AV nodes, as well as the aorta, pulmonary trunk, and coronary arteries 19-33

Nerve Supply to Heart Parasympathetics Parasympathetic stimulation:
Reduces heart rate Decreases contractility Increases Cardiac Output Parasympathetic Innervation: pathway begins with nuclei of the vagus nerves (CN X) in the medulla oblongata extend to cardiac plexus and continue to the heart by way of the cardiac nerves fibers of right vagus nerve lead to the SA node fibers of left vagus nerve lead to the AV node little or no vagal stimulation of the myocardium 19-33

Cardiac Rhythm Cycle of events in heart – special names
systole – atrial or ventricular contraction diastole – atrial or ventricular relaxation Sinus Rhythm - normal heartbeat triggered by the SA node set by SA node at 60 – 100 bpm adult at rest is 70 to 80 bpm (vagal tone) Ectopic Focus - another part of heart fires before SA node caused by hypoxia, electrolyte imbalance, caffeine, nicotine, and other drugs 19-34

Abnormal Heart Rhythms
Spontaneous firing from part of heart other than SA node ectopic foci - regions of spontaneous firing Nodal Rhythm – if SA node is damaged, heart rate is set by AV node, 40 to 50 bpm Intrinsic Ventricular Rhythm – if both SA and AV nodes are not functioning, rate set at 20 to 40 bpm this requires pacemaker to sustain life Arrhythmia – any abnormal cardiac rhythm failure of conduction system to transmit signals (heart block) bundle branch block total heart block (damage to AV node) 19-35

Cardiac Arrhythmias Atrial Flutter – ectopic foci in atria
atrial fibrillation atria beat times per minute Premature Ventricular Contractions (PVCs) caused by stimulants, stress or lack of sleep Ventricular Fibrillation serious arrhythmia caused by electrical signals reaching different regions at widely different times heart can’t pump blood and no coronary perfusion kills quickly if not stopped defibrillation - strong electrical shock whose intent is to depolarize the entire myocardium, stop the fibrillation, and reset SA nodes to sinus rhythm 19-36

Pacemaker Physiology The SA node spontaneously signals
The heart rhythm and contraction is automatic and originates in the heart itself Nervous stimulation can adjust heart contraction The SA node regularly signals The SA node is able to maintain a metronome like beat The rhythm is maintained through polarization and depolarization of the SA node cell membranes 19-37

Pacemaker Physiology The cell membrane maintains a Membrane Potential
Membrane Potential is an unequal charge between the inside and the outside of the membrane The membrane potential is maintained by ion channels regulating the flow of ions across the cell membrane Membrane potential is similar to a battery Just as a battery has positive and negative poles, so does the membrane (extracellular and intracellular poles) The cell membrane can conduct an electrical signal, just like a battery Polarization and Depolarization Polarization - the charge difference between the poles increases Depolarization - the charge difference between the poles equalizes 19-37

Pacemaker Physiology 1. Depolarization 2. Repolarization
Regular polarization and depolarization of the membrane regulates the cardiac rhythm: 1. Depolarization Depolarization has two stages: Gradual depolarization called the Pacemaker Potential Rapid depolarization facilitated by Fast Calcium-Sodium Ion Channels 2. Repolarization The resting membrane potential is restored 19-37

1. Depolarization The inside of the cell becomes less negative
Gradual depolarization called the Pacemaker Potential The resting membrane potential is -60 mV (The intracellular charge is negative compared to the outside) Na+ ions passively flow through ion channels into the cell The inside of the cell becomes less negative Rapid depolarization facilitated by Fast Calcium-Sodium Ion Channels When potenital reaches threshold of -40 mV, voltage-gated fast Ca2+ and Na+ channels open and ions rush into the cell Rapid Depolarization continues until the MP reaches 0 mV Each depolarization of the SA node sets off one heartbeat at rest, fires every 0.8 seconds or 75 bpm 19-37

1. Repolarization The RMP of -60 mV is restored
When the membrane depolarizes and the MP reaches 0 mV, K+ channels then open and K+ leaves the cell The intracellular charge becomes more negative causing repolarization to RMP -60 mV At RMP -60 mV, K+ channels close Pacemaker potential starts over as inflow of Na+ ions once again leads to the gradual depolarization of the Pacemaker Potential 19-37

SA Node Potentials Figure 19.13 Membrane potential (mV) Time (sec) +10
Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display. +10 –10 Fast K+ outflow Fast Ca2+–Na+ inflow Action potential –20 Membrane potential (mV) –30 Threshold –40 –50 Pacemaker potential –60 Slow Na+ inflow –70 .4 .8 1.2 1.6 Time (sec) Figure 19.13 19-38

Impulse Conduction to Myocardium
Signal from SA node stimulates L and R atria to contract almost simultaneously Signal delayed through AV node cardiocytes have fewer gap junctions delays signal 100 msec which allows ventricles to fill Signal travels through AV bundle and Purkinje fibers ventricular myocardium depolarizes and contracts in near unison papillary muscles contract tightening chordae tendineae closing AV valves Ventricular systole progresses up from the apex spiral arrangement of cardiocytes ‘wrings’ out ventricles 19-39

Myocardiocyte Physiology
Cardiocytes have a stable RMP of - 90 mV cadiocyte Na+ ion channels are voltage gated, do not ‘leak’ like SA node Na+ ion channels depolarize only when stimulated Three phases of Mycardiocyte Contraction: Depolarization Phase Plateau Phase Repolarization Phase 19-40

Myocardiocyte Physiology
Depolarization Phase nodal stimulus opens voltage regulated Na+ gates, Na+ rushes in, membrane depolarizes rapidly Na+ gates close quickly at +30 mV Plateau Phase Ca2+ channels are slow to close and SR is slow to uptake Ca2+ from the cytosol sustains contraction for expulsion of blood from heart lasts 200 to 250 msec Repolarization Phase Ca2+ channels close, K+ channels open rapid diffusion of K+ out of cell returns it to resting potential 19-40

Action Potential of a Cardiocyte
Na+ gates open 2) Rapid depolarization 3) Na+ gates close 4) Slow Ca2+ channels open 5) Ca2+ channels close, K+ channels open (repolarization) Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display. 3 1 Plateau Voltage-gated Na+ channels open. +20 4 2 Na+ inflow depolarizes the membrane and triggers the opening of still more Na+ channels, creating a positive feedback cycle and a rapidly rising membrane voltage. Action potential 5 3 Na+ channels close when the cell depolarizes, and the voltage peaks at nearly +30 mV. –20 Myocardial relaxation Membrane potential (mV) 4 Ca2+ entering through slow Ca2+ channels prolongs depolarization of membrane, creating a plateau. Plateau falls slightly because of some K+ leakage, but most K+ channels remain closed until end of plateau. –40 2 Myocardial contraction –60 Absolute refractory period 5 Ca2+ channels close and Ca2+ is transported out of cell. K+ channels open, and rapid K+ outflow returns membrane to its resting potential. –80 1 .15 .30 Time (sec) Figure 19.14 19-41

Action Potential of a Cardiocyte
Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display. Long absolute refractory period 250 msec compared to 1 – 2 msec in skeletal muscle prevents wave summation and tetanus which would stop the pumping action of the heart 3 1 Plateau Voltage-gated Na+ channels open. +20 4 2 Na+ inflow depolarizes the membrane and triggers the opening of still more Na+ channels, creating a positive feedback cycle and a rapidly rising membrane voltage. Action potential 5 3 Na+ channels close when the cell depolarizes, and the voltage peaks at nearly +30 mV. –20 Myocardial relaxation Membrane potential (mV) 4 Ca2+ entering through slow Ca2+ channels prolongs depolarization of membrane, creating a plateau. Plateau falls slightly because of some K+ leakage, but most K+ channels remain closed until end of plateau. –40 2 Myocardial contraction –60 Absolute refractory period 5 Ca2+ channels close and Ca2+ is transported out of cell. K+ channels open, and rapid K+ outflow returns membrane to its resting potential. –80 1 .15 .30 Time (sec) Figure 19.14 19-41

Electrocardiogram (ECG or EKG)
composite of all action potentials of nodal and myocardial cells detected, amplified and recorded by electrodes on arms, legs and chest Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display. 0.8 second R R +1 PQ segment ST segment T wave Millivolts P wave PR interval Q S QT interval Figure 19.15 QRS interval –1 Atria contract Ventricles contract Atria contract Ventricles contract 19-42

ECG Deflections P wave QRS complex ST segment - ventricular systole
SA node fires, atria depolarize and contract atrial systole begins 100 msec after SA signal QRS complex ventricular depolarization complex shape of spike due to different thickness and shape of the two ventricles ST segment - ventricular systole plateau in myocardial action potential T wave ventricular repolarization and relaxation 19-43

Electrical Activity of Myocardium
atrial depolarization begins 2) atrial depolarization complete (atria contracted) ventricles begin to depolarize at apex; atria repolarize (atria relaxed) ventricular depolarization complete (ventricles contracted) ventricles begin to repolarize at apex 6) ventricular repolarization complete (ventricles relaxed) Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display. Key Wave of depolarization Wave of repolarization R P P Q S 1 Atria begin depolarizing. 4 Ventricular depolarization complete. R P P T Q S 2 Atrial depolarization complete. 5 Ventricular repolarization begins at apex and progresses superiorly. R R P P T Q Q S 3 Ventricular depolarization begins at apex and progresses superiorly as atria repolarize. 6 Ventricular repolarization complete; heart is ready for the next cycle. Figure 19.16 19-45

Normal Electrocardiogram (ECG)
Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display. 0.8 second R R +1 PQ segment ST segment P wave T wave Millivolts PR interval Q S QT interval QRS interval –1 Atria contract Ventricles contract Atria contract Ventricles contract Figure 19.15 19-44

Diagnostic Value of ECG
Abnormalities in conduction pathways Myocardial infarction Nodal damage Heart enlargement Electrolyte and hormone imbalances 19-46

Cardiac Cycle Cardiac Cycle - one complete contraction and relaxation of all four chambers of the heart Atrial systole (contraction) occurs while ventricles are in diastole (relaxation) Atrial diastole occurs while ventricles in systole Quiescent Period all four chambers relaxed at same time questions to solve – how does pressure affect blood flow? and how are heart sounds produced? 19-48

Principles of Pressure and Flow
Two main variables that govern fluid movement: Pressure - causes a fluid to flow (fluid dynamics) pressure gradient - pressure difference between two points measured sphygmomanometer Resistance - opposes fluid flow great vessels have positive blood pressure ventricular pressure must rise above this resistance for blood to flow into great vessels Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display. 1 Volume increases 2 Pressure decreases 3 Air flows in P1 P2>P1 P2 Pressure gradient (a) 1 Volume decreases 2 Pressure increases 3 Air flows out P1 P2<P1 Pressure gradient (b) P2 19-49 Figure 19.18

Pressure Gradients and Flow
Fluid only flows down its pressure gradient from high pressure to low pressure Events occurring on left side of heart when ventricle relaxes and expands, its internal pressure falls if bicuspid valve is open, blood flows into left ventricle when ventricle contracts, internal pressure rises AV valves close and 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 19-50

Operation of Heart Valves
Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display. Atrium Atrioventricular valve Ventricle Atrioventricular valves open Atrioventricular valves closed (a) Figure 19.19 Aorta Pulmonary artery Semilunar valve 19-51 Semilunar valves open Semilunar valves closed (b)

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 result of rheumatic fever autoimmune attack on the mitral and aortic valves heart overworks and may become enlarged Mitral Valve Prolapse – insufficiency in which one or both mitral valve cusps bulge into atria during ventricular contraction hereditary in 1 out of 40 people may cause chest pain and shortness of breath Heart Murmur – abnormal heart sound produced by regurgitation of blood through incompetent valves 19-52

Heart Sounds Auscultation - listening to sounds made by body
Two stages of heart sounds First Heart Sound (S1) louder and longer “lubb” occurs with closure of AV valves Second Heart Sound (S2) softer and sharper “dupp” occurs with closure of semilunar valves 19-53

Cardiac Cycle Four Phases of Cardiac Cycle
Ventricular Filling Isovolumetric Contraction Ventricular Ejection Isovolumetric Relaxation Total duration of the cardiac cycle is 0.8 sec in a heart beating 75 bpm 19-54

1. Ventricular Filling During diastole, ventricles expand
their pressure drops below that of the atria AV valves open and blood flows into the ventricles Ventricular filling occurs in three phases: rapid ventricular filling - first one-third blood enters very quickly diastasis - second one-third marked by slower filling P wave occurs at the end of diastasis atrial systole - final one-third atria contract End-diastolic volume (EDV) – amount of blood contained in each ventricle at the end of ventricular filling 130 mL of blood 19-55

2. Isovolumetric Contraction
Atria repolarize and relax remain in diastole for the rest of the cardiac cycle Ventricles depolarize, create the 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 ‘Isovolumetric’ because even though the ventricles contract, they do not eject blood because pressure in the aorta (80 mm Hg) and in pulmonary trunk (10 mm Hg) is still greater than in the ventricles Cardiocytes exert force, but with all four valves closed, the blood cannot go anywhere 19-56

3. Ventricular Ejection Ejection of blood begins when the ventricular pressure exceeds arterial pressure and forces semilunar valves open pressure peaks in left ventricle at about 120 mm Hg and 25 mm Hg in the right Blood spurts out of each ventricle rapidly at first – rapid ejection then more slowly under reduced pressure – reduced ejection ventricular ejections last about 200 – 250 msec corresponds to the plateau phase of the cardiac action potential T wave occurs late in this phase stroke volume (SV) of about 70 mL of blood is ejected of the 130 mL in each ventricle ejection fraction of about 54% as high as 90% in vigorous exercise end-systolic volume (ESV) – the 60 mL of blood left behind 19-57

4. Isovolumetric Relaxation
early ventricular diastole when T wave ends and the ventricles begin to expand elastic recoil and expansion would cause pressure to drop rapidly and suck blood into the ventricles blood from the aorta and pulmonary briefly flows backwards filling the semilunar valves and closing the cusps creates a slight pressure rebound that appears as the dicrotic notch of the aortic pressure curve heart sound S2 occurs as blood rebounds from the closed semilunar valves and the ventricle expands ‘isovolumetric’ because semilunar valves are closed and AV valves have not yet opened ventricles are therefore taking in no blood when AV valves open, ventricular filling begins again 19-58

Major Events of Cardiac Cycle
Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display. Diastole Systole Diastole 120 Aortic pressure ventricular filling isovolumetric contraction ventricular ejection isovolumetric relaxation 100 80 Aortic valve opens Aortic valve closes (dicrotic notch) Left ventricular pressure Pressure (mm Hg) 60 40 AV valve closes AV valve opens Left atrial pressure 20 120 End-diastolic volume Ventricular volume (mL) 90 60 End-systolic volume R R P T P ECG Q Q S S Heart sounds S2 S3 S1 S2 S3 S1 Phase of cardiac cycle 1a 1b 1c 2 3 4 1a 1b 1c 2 .2 .4 .6 .8 .2 .4 Time (sec) Ventricular filling 2 Isovolumetric contraction 3 Ventricular ejection 4 Isovolumetric relaxation 1a Rapid filling 1b Diastasis 1c Atrial systole Figure 19.20 19-60

Unbalanced Ventricular Output
Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display. 1 Right ventricular output exceeds left ventricular output. 2 Pressure backs up. pulmonary edema 3 Fluid accumulates in pulmonary tissue. 1 2 3 Figure 19.21a 19-62 (a) Pulmonary edema

Unbalanced Ventricular Output
Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display. 1 Left ventricular output exceeds right ventricular output. 2 Pressure backs up. peripheral edema 3 Fluid accumulates in systemic tissue. 2 1 Figure 19.21b 3 19-63 (b) Systemic edema

Congestive Heart Failure
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. Left Ventricular Failure – blood backs up into the lungs causing pulmonary edema shortness of breath or sense of suffocation Right Ventricular Failure – blood backs up in the vena cava causing systemic or generalized edema enlargement of the liver, ascites (pooling of fluid in abdominal cavity), distension of jugular veins, swelling of the fingers, ankles, and feet Leads to total heart failure 19-64

Cardiac Output = Heart Rate x Strove Volume
Cardiac Output (CO) Cardiac Output (CO) – the amount ejected by ventricle in 1 minute about 4 to 6 L/min at rest CO = HR x SV Cardiac Output = Heart Rate x Strove Volume Cardiac Output is directly proportional the Heat Rate and Stroke Volume Cardiac Reserve – the difference between a person’s maximum and resting CO increases with fitness, decreases with disease 19-65

Heart Rate Pulse – surge of pressure produced by each heart beat that can be felt by palpating a superficial artery with the fingertips infants have HR of 120 bpm or more young adult females avg bpm young adult males avg. 64 to 72 bpm heart rate rises again in the elderly Tachycardia - resting adult heart rate above 100 bpm stress, anxiety, drugs, heart disease, or fever loss of blood or damage to myocardium Bradycardia - resting adult heart rate of less than 60 bpm in sleep, low body temperature, and endurance trained athletes positive chronotropic agents – factors that raise the heart rate negative chronotropic agents – factors that lower heart rate 19-66

Chronotropic Effects of the Autonomic Nervous System
Cardiac Centers in the Reticular Formation of the Medulla Oblongata initiate autonomic output to the heart Cardiostimulatory Effect – some neurons of the cardiac center transmit signals to the heart by way of sympathetic pathways Cardioinhibitory Effect – others transmit parasympathetic signals by way of the vagus nerve 19-67

Chronotropic Effects of the ANS
Sympathetic postganglionic fibers (Adrenergic) Release norepinephrine Binds to β-adrenergic fibers in the heart Activates c-AMP second-messenger system in cardiocytes and nodal cells Leads to opening of Ca2+ channels in plasma membrane Increased Ca2+ inflow accelerates depolarization of SA node cAMP accelerates the uptake of Ca2+ by the sarcoplasmic reticulum allowing the cardiocytes to relax more quickly by accelerating both contraction and relaxation, norepinephrine and cAMP increase the heart rate as high as 230 bpm diastole becomes too brief for adequate filling both stroke volume and cardiac output are reduced 19-68

Chronotropic Effects of the ANS
Parasympathetic Vagus Nerves (Cholinergic) inhibitory effects on the SA and AV nodes Acetylcholine (ACh) binds to muscarinic receptors opens K+ gates in the nodal cells as K+ leaves the cells, they become hyperpolarized and fire less frequently heart slows down Parasympathetics do not need a second messenger system Vagal Tone – holds down heart rate to 70 – 80 bpm at rest steady background firing rate of the vagus nerves without influence from the cardiac centers, the heart has a intrinsic “natural” firing rate of 100 bpm 19-69

Inputs to Cardiac Center
Cardiac centers in the Medulla receive input from many sources and integrate it into the ‘decision’ to speed or slow the heart Medulla receives input from muscles, joints, arteries, and brainstem Proprioceptors in the muscles and joints inform cardiac center about changes in activity, HR increases before metabolic demands of muscle arise Paroreceptors signal cardiac center pressure sensors in aorta and internal carotid arteries blood pressure decreases, signal rate drops, cardiac center increases heart rate if blood pressure increases, signal rate rises, cardiac center decreases heart rate 19-70

Higher Brain Centers affect heart rate cerebral cortex, limbic system, hypothalamus sensory or emotional stimuli

Chemoreceptors in aortic arch, carotid arteries and medulla oblongata sensitive to blood pH, CO2 and O2 levels more important in respiratory control than cardiac control if CO2 accumulates in blood or CSF (hypercapnia), reacts with water and causes increase in H+ levels H+ lowers the pH of the blood possibly creating acidosis (pH < 7.35) hypercapnia and acidosis stimulate the cardiac center to increase heart rate also respond to hypoxemia – oxygen deficiency in the blood usually slows down the heart chemoreflexes and baroreflexes, responses to fluctuation in blood chemistry, are both negative feedback loops 19-71

Chronotropic Chemicals
Chemicals affect heart rate as well as neurotransmitters from cardiac nerves blood born adrenal catecholamines (NE and epinephrine) are potent cardiac stimulants Drugs that stimulate heart nicotine stimulates catecholamine secretion thyroid hormone increases number adrenergic receptors on heart so more responsive to sympathetic stimulation caffeine inhibits cAMP breakdown prolonging adrenergic effect 19-72

Chronotropic Chemicals
Electrolytes K+ has greatest chronotropic effect hyperkalemia – excess K+ in cardiocytes myocardium less excitable, heart rate slows and becomes irregular hypokalemia – deficiency K+ in cardiocytes cells hyperpolarized, require increased stimulation Calcium hypercalcemia – excess of Ca2+ decreases heart rate and contraction strength hypocalcemia – deficiency of Ca2+ increases heart rate and contraction strength 19-73

Stroke Volume (SV) CO = HR x SV SV = EDV - ESV
Cardiac Output = Heart Rate x Strove Volume Three variables govern stroke volume: Preload Contractility Afterload SV = EDV - ESV Stroke Volume = End Diastolic Volume - End Systolic Volume EDV = Capacity of blood before LV systole EVS = Capacity of blood left in LV after systole 19-74

Stroke Volume = End Diastolic Volume - End Systolic Volume
Stroke Volume (SV) SV = EDV - ESV Stroke Volume = End Diastolic Volume - End Systolic Volume EDV = Capacity of blood before LV systole EVS = Capacity of blood left in LV after systole Factors that increase EDV and reduce ESV increase stroke volume and CO increased preload or contractility causes increases stroke volume increased afterload causes decrease stroke volume

1. Preload Preload – the amount of tension in ventricular myocardium immediately before it begins to contract increased preload causes increased force of contraction exercise increases venous return and stretches myocardium cardiocytes generate more tension during contraction increased cardiac output matches increased venous return Frank-Starling law of heart - SV∝ EDV stroke volume is proportional to the end diastolic volume ventricles eject as much blood as they receive the more they are stretched, the harder they contract 19-75

2. Contractility Contractility refers to how hard the myocardium contracts for a given preload Positive Inotropic Agents increase contractility hypercalcemia can cause strong, prolonged contractions and even cardiac arrest in systole catecholamines increase calcium levels glucagon stimulates cAMP production digitalis raises intracellular calcium levels and contraction strength Negative Inotropic Agents reduce contractility hypocalcemia can cause weak, irregular heartbeat and cardiac arrest in diastole hyperkalemia (high K+) reduces strength of myocardial action potentials and the release of Ca2+ into the sarcoplasm vagus nerves have effect on atria but too few nerves to ventricles for a significant effect 19-76

3. Afterload Afterload – the blood pressure in the aorta and pulmonary trunk immediately distal to the semilunar valves opposes the opening of these valves limits stroke volume Hypertension (High peripheral Blood Pressure increases afterload and opposes ventricular ejection Anything that impedes arterial circulation can also increase afterload lung diseases that restrict pulmonary circulation cor pulmonale – right ventricular failure due to obstructed pulmonary circulation in emphysema, chronic bronchitis, and black lung disease 19-77

How to Prepare for the Practical
Read and Review Chapter 19, images, and the Lecture Slides Read and Review Chapter 19 Lab Handout and Slides ID the anatomical structures listed on your lab handout Review blood flow Review Resources Review anatomical models and software in LC Come prepared for WET LAB Please see me if you object to conducting dissections or handling pigs

Chapter 19: The Circulatory System: The Heart

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Chapter 19: The Circulatory System: The Heart

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