the heart chapter 20. function of the heart pumping the red stuff anatomy of the heart location –...
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The Heart
Chapter 20
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Function of the Heart• Pumping the red stuff
Anatomy of the Heart• Location – mediastinum, slightly to the left
of center
• Size – about that of your fist
• Mass – 250 – 300 g
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Organization of the
Cardiovascular System
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Location
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Tissues of the Heart
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Coverings of the Heart: Anatomy
• Pericardium – a double-walled sac around the heart composed of:– A superficial fibrous pericardium– A deep two-layer serous pericardium
• The parietal layer lines the internal surface of the fibrous pericardium
• The visceral layer or epicardium lines the surface of the heart
• They are separated by the fluid-filled pericardial cavity
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Coverings of the Heart: Physiology
• The pericardium:– Protects and anchors the heart– Prevents overfilling of the heart with blood– Allows for the heart to work in a relatively
friction-free environment
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Serous pericardium
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General Anatomy
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Heart Wall
• Epicardium – visceral layer of the serous pericardium
• Myocardium – cardiac muscle layer forming the bulk of the heart
• Fibrous skeleton of the heart – crisscrossing, interlacing layer of connective tissue
• Endocardium – endothelial layer of the inner myocardial surface
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• Vessels returning blood to the heart include:– Superior and inferior venae cavae– Right and left pulmonary veins
• Vessels conveying blood away from the heart include:– Pulmonary trunk, which splits into right and left
pulmonary arteries– Ascending aorta (three branches) – brachiocephalic,
left common carotid, and subclavian arteries
External Heart: Major Vessels of the Heart (Anterior View)
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• Arteries – right and left coronary (in atrioventricular groove), marginal, circumflex, and anterior interventricular arteries
• Veins – small cardiac, anterior cardiac, and great cardiac veins
External Heart: Vessels that Supply/Drain the Heart (Anterior View)
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Surface features of the heart
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Cardiac Muscle CellsFigure 20–5
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• Vessels returning blood to the heart include:– Right and left pulmonary veins– Superior and inferior venae cavae
• Vessels conveying blood away from the heart include:– Aorta– Right and left pulmonary arteries
External Heart: Major Vessels of the Heart (Posterior View)
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Posterior view
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Atria of the Heart
• Atria are the receiving chambers of the heart
• Each atrium has a protruding auricle
• Pectinate muscles mark atrial walls
• Blood enters right atria from superior and inferior venae cavae and coronary sinus
• Blood enters left atria from pulmonary veins
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Deep in your heart of hearts…
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Ventricles of the Heart
• Ventricles are the discharging chambers of the heart
• Papillary muscles and trabeculae carneae muscles mark ventricular walls
• Right ventricle pumps blood into the pulmonary trunk
• Left ventricle pumps blood into the aorta
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Note the differences in wall thickness
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Heart Valves
• Heart valves ensure unidirectional blood flow through the heart
• Atrioventricular (AV) valves lie between the atria and the ventricles
• AV valves prevent backflow into the atria when ventricles contract
• Chordae tendineae anchor AV valves to papillary muscles
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Heart Valves
• Aortic semilunar valve lies between the left ventricle and the aorta
• Pulmonary semilunar valve lies between the right ventricle and pulmonary trunk
• Semilunar valves prevent backflow of blood into the ventricles
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The heart valves
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Function of the bicuspid valve
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Valve functions
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Heart Sounds
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Where to go to listen to heart sounds
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Some heart valve disorders• Stenosis (narrowing) – the inability of a valve to
open fully
• Insufficiency (incompetence) – failure of the valve to prevent back flow or close properly– Mitral valve prolapse – one or both of the flaps
blows back into the atrium during systole (contraction) of the ventricle allowing backflow into the atrium.
– The aortic semilunar valves can also suffer from stenosis or insufficiency, allowing backflow into the ventricle.
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Pathway of Blood Through the Heart and Lungs
• Right atrium tricuspid valve right ventricle
• Right ventricle pulmonary semilunar valve pulmonary arteries lungs
• Lungs pulmonary veins left atrium
• Left atrium bicuspid valve left ventricle
• Left ventricle aortic semilunar valve aorta
• Aorta systemic circulation
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Systemic & pulmonary circuits
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Blood flow
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Coronary Circulation
• Coronary circulation is the functional blood supply to the heart muscle itself
• Collateral routes ensure blood delivery to heart even if major vessels are occluded
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Coronary Circulation
(arterial)
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Coronary Circulation
(venous)
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Cardiac histology & physiology• Cardiac muscle is made of short, branched
fibers
• Striated
• Uninucleate
• There is now some evidence that it has limited mitotic capability (it is likely that regeneration is from migration of stem cells from the blood)
• 99% are contractile
• 1% are “autorhythmic” or “pacemaker” cells
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Cardiac Muscle Tissue
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Cardiac Muscle Cells
• Intercalated discs:– interconnect cardiac muscle cells– secured by desmosomes – linked by gap junctions– convey force of contraction – propagate action potentials
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Characteristics of Cardiac Muscle Cells
1. Small size
2. Single, central nucleus
3. Branching interconnections between cells
4. Intercalated discs
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Cardiac Cells vs. Skeletal Fibers Table 20-1
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The intrinsic conduction system
• Sinoatrial node: the primary pacemaker – has an intrinsic firing rate of about 100 bpm but kept at 60 – 80 by parasympathetic tone
• Generates pacemaker potentials from leakage of Ca++
• Depolarization spreads via gap junctions in intercalated disks
• Rate can be adjusted by ANS
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Intrinsic conduction system • Signals from SA node travel to the
Atrioventricular Node via the internodal pathway
• The AV node has its own intrinsic firing rate of 40 – 60 bpm. In absence of SA node function it can establish a “junctional rhythm” that keeps the ventricles working
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The conducting pathways
• The signal is delayed about 0.1 s and then transmitted down the …
• Bundle of His or AV bundle and the left & right bundle branches to the apex
• And from there the depolarization is distributed by the Purkinje fibers
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Fig. 20.10a
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Contraction of cardiac muscle fibersand the cardiac cycle
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The ElectrocardiogramFigure 20–14b
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NSR:Normal Sinus
Rhythm
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Prolonged contraction of cardiac muscle
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Features of an ECG
• P wave:
– atria depolarize
• QRS complex:
– ventricles depolarize
• T wave:
– ventricles repolarize
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Resting Potential
• Of a ventricular cell:
–about —90 mV
• Of an atrial cell:
–about —80 mV
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3 Steps of Cardiac Action Potential
1.Rapid depolarization:
» voltage-regulated sodium channels (fast channels) open
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3 Steps of Cardiac Action Potential
2. As sodium channels close:
– voltage-regulated calcium channels (slow channels) open
– balance Na+ ions pumped out
– hold membrane at 0 mV plateau
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3 Steps of Cardiac Action Potential
3. Repolarization:
– plateau continues
– slow calcium channels close
– slow potassium channels open
– rapid repolarization restores resting potential
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The Refractory Periods
• Absolute refractory period:
– long
– cardiac muscle cells cannot respond
• Relative refractory period:
– short
– response depends on degree of stimulus
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Timing of Refractory Periods
• Length of cardiac action potential in ventricular cell:– 250–300 msecs
• 30 times longer than skeletal muscle fiber• long refractory period prevents summation
and tetany
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ElectricalActivity and the Cardiac Cycle
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Calcium and Contraction
• Contraction of a cardiac muscle cell is produced by an increase in calcium ion concentration around myofibrils
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2 Steps of Calcium Ion Concentration
1. 20% of calcium ions required for a contraction:
– calcium ions enter cell membrane during plateau phase
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2 Steps of Calcium Ion Concentration
2. Arrival of extracellular Ca2+:– triggers release of calcium ion reserves from
sarcoplasmic reticulum
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Intracellular and Extracellular Calcium
• As slow calcium channels close:– intracellular Ca2+ is absorbed by the SR– or pumped out of cell
• Cardiac muscle tissue:– very sensitive to extracellular Ca2+
concentrations
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The Cardiac Cycle
• CO is the amount of blood pumped by each ventricle in one minute
• CO is the product of heart rate (HR) and 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
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Phases of the Cardiac CycleFigure 20–16
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Cardiac output
• CO (ml/min) = HR (75 beats/min) x SV (70 ml/beat)• CO = 5250 ml/min (5.25 L/min)
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Cardiac output
• SV = 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
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Pressure and
Volume in the
Cardiac Cycle
Figure 20–17
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Factors Affecting Stroke Volume
• Preload – amount ventricles are stretched by contained blood
• Contractility – cardiac cell contractile force due to factors other than EDV
• Afterload – back pressure exerted by blood in the large arteries leaving the heart
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Factors Affecting Stroke Volume
• Changes in EDV or ESV
Figure 20–23 (Navigator)
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Frank-Starling Law of the Heart
• Preload, or degree of stretch, of cardiac muscle cells before they contract is the critical factor controlling stroke volume
• Slow heartbeat and exercise increase venous return to the heart, increasing SV
• Blood loss and extremely rapid heartbeat decrease SV
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Extrinsic Factors Influencing Stroke Volume
• Contractility is the increase in contractile strength, independent of stretch and EDV
• Increase in contractility comes from: – Increased sympathetic stimuli– Certain hormones– Ca2+ and some drugs
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Factors Affecting Heart Rate and Stroke Volume
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Extrinsic Factors Influencing Stroke Volume
• Agents/factors that decrease contractility include:– Acidosis– Increased extracellular K+
– Calcium channel blockers
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Contractility and Norepinephrine
• Sympathetic stimulation releases norepinephrine and initiates a cyclic AMP second-messenger system
Figure 18.22
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Regulation of Heart Rate
• Positive chronotropic factors increase heart rate
• Negative chronotropic factors decrease heart rate
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• Sympathetic nervous system (SNS) stimulation is activated by stress, anxiety, excitement, or exercise
• Parasympathetic nervous system (PNS) stimulation is mediated by acetylcholine and opposes the SNS
• PNS dominates the autonomic stimulation, slowing heart rate and causing vagal tone
Regulation of Heart Rate: Autonomic Nervous System
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Autonomic Innervation
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Autonomic Pacemaker Regulation
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Autonomic Pacemaker Regulation (1 of 3)
• Sympathetic and parasympathetic stimulation:– greatest at SA node (heart rate)
• Membrane potential of pacemaker cells:– lower than other cardiac cells
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Autonomic Pacemaker Regulation (2 of 3)
• Rate of spontaneous depolarization depends on:– resting membrane potential– rate of depolarization
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Autonomic Pacemaker Regulation (3 of 3)
• ACh (parasympathetic stimulation):– slows the heart
• NE (sympathetic stimulation):– speeds the heart
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Atrial (Bainbridge) Reflex
• Atrial (Bainbridge) reflex – a sympathetic reflex initiated by increased blood in the atria– Causes stimulation of the SA node– Stimulates baroreceptors in the atria,
causing increased SNS stimulation
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CNS and ANS controls of Cardiac output
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Chemical Regulation of the Heart
• The hormones epinephrine and thyroxine increase heart rate
• Intra- and extracellular ion concentrations must be maintained for normal heart function
InterActive Physiology®: Cardiovascular System: Cardiac OutputPLAYPLAY
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Factors Involved in Regulation of Cardiac Output
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How the heart starts
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Examples of Congenital Heart Defects
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Congestive Heart Failure (CHF)
• Congestive heart failure (CHF) is caused by:– Coronary atherosclerosis– Persistent high blood pressure– Multiple myocardial infarcts– Dilated cardiomyopathy (DCM)
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Arteriosclerosis
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Fig. 20.20
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Age-Related Changes Affecting the Heart
• Sclerosis and thickening of valve flaps
• Decline in cardiac reserve
• Fibrosis of cardiac muscle
• Atherosclerosis