Download Cardiac Physiology

The Cardiovascular System
Cardiac Physiology
Keri Muma
Bio 6
  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
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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
 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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Copyright © 2004 Pearson Education, Inc., publishing as Benjamin Cummings
1
Intrinsic Conduction System
Intrinsic Conduction System
  Sequence of Excitation
  The action potential generated by autorhythmic cells
travel through the conduction system and to
surrounding myocardial tissue by gap junction
  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
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Pacemaker and Action Potentials of the Heart
  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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Copyright © 2004 Pearson Education, Inc., publishing as Benjamin Cummings
Figure 18.13
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Electrocardiography
  EKG – tracing of the electrical currents created by
the intrinsic conduction system
  Test to screen for a variety of cardiac abnormalities
Electrocardiography
  P wave – atrial
depolarization
  QRS complex –
ventricles depolarization
  T wave – ventricles
repolarization
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Copyright © 2004 Pearson Education, Inc., publishing as Benjamin Cummings
Cardiac Abnormalities
  Bradycardia - <60 BPM
  Tachycardia - >100 BPM
  Arrhythmias – uncoordinated atrial and ventricular
contractions
  Damaged SA node – pace set by AV node ~ 50
BPM
  Heart block – damage to the AV node, ventricles
contract at ~30 BPM
  Fibrillation – irregular chaotic twitching of the
myocardium
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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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Copyright © 2004 Pearson Education, Inc., publishing as Benjamin Cummings
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Action potentials in Cardiac Muscle Cells
Comparison of Action Potentials
  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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Contraction of Cardiac Muscle
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Metabolism 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
  Relies almost exclusively on aerobic respiration
  The Ca2+ influx induces
the release of additional
Ca2+ from the SR
  Adaptive to multiple fuel sources: glucose, fatty
acids, lactic acid)
  Constant and adequate blood supply is critical
  Ca2+ binds to troponin
allowing sliding of the
myofilaments
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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
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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
  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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Copyright © 2004 Pearson Education, Inc., publishing as Benjamin Cummings
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Phases of the Cardiac Cycle
  Ventricular systole
  Atrial diastole
Phases of the Cardiac Cycle
  Isovolumetric relaxation – early diastole
  Ventricles relax
  Rising ventricular pressure results in closing of AV valves
  Backflow of blood in aorta and pulmonary trunk closes
semilunar valves
  Isovolumetric contraction phase
  Atria re-filling
  Ventricular ejection phase opens semilunar valves
  Atria pressure increases, AV valves open and cycle repeats
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Heart Sounds
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Operation of AV Valves
  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 SL Valves
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Summary:
Figure 18.20
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Cardiac Output (CO) and Reserve
Cardiac Output: Example
  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
  CO (ml/min) = HR (75 beats/min) x SV (70 ml/beat)
  CO = 5250 ml/min (5.25 L/min)
  Cardiac reserve is the difference between resting and
maximal CO
Copyright © 2004 Pearson Education, Inc., publishing as Benjamin Cummings
Copyright © 2004 Pearson Education, Inc., publishing as Benjamin Cummings
Regulation of Heart Rate
  Heart rate is modulated by the
autonomic nervous system
  Parasympathetic activity –
slows HR down via ACh
  Increases K+ permeability,
hyperpolarization
  Sympathetic activity–increases
HR via NE/E
  Increases Na+, and Ca2+
channels, speeds up
depolarization
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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
  Chronotropic agents –
affect heart rate
  Positive chronotropic
factors increase heart
rate
  Negative
chronotropic factors
decrease heart rate
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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
  Age – decreases HR
  Exercise – increases HR
  Temperature – increases HR
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Copyright © 2004 Pearson Education, Inc., publishing as Benjamin Cummings
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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:
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
  Exercise
  Slower heart beat
  Factors that would decrease preload
  Blood loss
  Rapid heart beat
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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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Extrinsic Factors Influencing Stroke Volume
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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
Factors Affecting Cardiac Output
  Agents/factors that decrease contractility include:
  Acidosis
  Increased extracellular Na+ and K+
  Calcium channel blockers
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Factors Involved in Regulation of Cardiac Output
Figure 18.23
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