Download Intrinsic Conduction System

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
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Gross Anatomy of the Heart
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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
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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
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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
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Intrinsic Conduction System
 The action potential generated by autorhythmic cells
travel through the conduction system and to
surrounding myocardial tissue by gap junction
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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)
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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)
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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
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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
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Pacemaker and Action Potentials of the Heart
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Figure 18.13
Electrocardiography
 EKG – tracing of the electrical currents created by
the intrinsic conduction system
 Test to screen for a variety of cardiac abnormalities
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Electrocardiography
 P wave – atrial
depolarization
 QRS complex –
ventricles depolarization
 T wave – ventricles
repolarization
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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
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Copyright © 2004 Pearson Education, Inc., publishing as Benjamin Cummings
Cardiac Abnormalities
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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
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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
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Comparison of Action Potentials
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Contraction of Cardiac Muscle
 Cardiac muscle contraction is
similar to skeletal muscle
contraction
 The action potential
traveling down the Ttubules 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
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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)
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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
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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
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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
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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
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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
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Operation of AV Valves
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Operation of SL Valves
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Summary:
Figure 18.20
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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
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Cardiac Output: Example
 CO (ml/min) = HR (75 beats/min) x SV (70 ml/beat)
 CO = 5250 ml/min (5.25 L/min)
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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
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Regulation of Heart Rate
 Chronotropic agents –
affect heart rate
 Positive chronotropic
factors increase heart
rate
 Negative
chronotropic factors
decrease heart rate
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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
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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
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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
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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 Ca2+ and some drugs like digitalis
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Contractility and Norepinephrine
 Sympathetic
stimulation
releases
norepinephrine
and initiates a
cyclic AMP
secondmessenger
system
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Figure 18.22
Extrinsic Factors Influencing Stroke Volume
 Agents/factors that decrease contractility include:
 Acidosis
 Increased extracellular Na+ and K+
 Calcium channel blockers
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Factors Affecting Cardiac Output
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Factors Involved in Regulation of Cardiac Output
Figure 18.23
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