Download Cardiac muscle contraction

PowerPoint® Lecture Slides
prepared by
Janice Meeking,
Mount Royal College
CHAPTER
18
The
Cardiovascular
System: The
Heart: Part B
Copyright © 2010 Pearson Education, Inc.
Cardiac Cycle
• Cardiac cycle - The period between the start of one heartbeat
and the beginning of the next.
• During the cycle, each of the four chambers goes through
• Systole – contraction of heart muscle
• Diastole – relaxation of heart muscle
• An average heart beat (HR)/cardiac cycle is 75 bpm. That
means that a cardiac cycle length is about 0.8 second.
• Of that 0.1 second is the atrial contraction, 0.3 is the atrial
relaxation and ventricular contraction.
• The remaining 0.4 seconds are the ventricular relaxation
• The cardiac cycle creates pressure gradient that maintains
blood flow
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Phases of the Cardiac Cycle and pressure gradient
80% of blood
flows passively
into the
ventricles
Figure 20.16
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The conductive system
• The heart is an autonomic system that can work
without neural stimuli – an intrinsic conduction
system.
• The autonomic function of the heart results from:
• The pacemaker function – Autorhythmic cells
• The conductive system that transfer those impulses
throughout the heart
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Conduction pathways in the heart
•
The upper part of the heart (the 2 atria) is insulated from
the lower part
•
Sinoatrial (SA) node (pacemaker)
•
Generates impulses about 75 times/minute (sinus rhythm)
•
Depolarizes faster than any other part of the myocardium
•
Atrioventricular (AV) node
•
Smaller diameter fibers; fewer gap junctions
•
Delays impulses approximately 0.1 second
•
Depolarizes 50 times per minute in absence of SA node
input
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Heart Physiology: Sequence of Excitation
•
Atrioventricular (AV) bundle (bundle of His)
•
•
Only electrical connection between the atria and
ventricles
Right and left bundle branches
•
•
Two pathways in the interventricular septum that
carry the impulses toward the apex of the heart
Purkinje fibers
•
Complete the pathway into the apex and ventricular
walls
•
AV bundle and Purkinje fibers depolarize only
30 times per minute in absence of AV node input
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Electrocardiography (ECG or EKG)
• Body fluids are good conductors which allows the
record of the myocardial action potential extracellularly
• EKG pairs of electrodes (leads) one serve as positive
side of the lead and one as the negative
• Potentials (voltage) are being measured between the 2
electrodes
• EKG is the summed electrical potentials generated by
all cells of the heart and gives electrical “view” of 3D
object (different from one action potential)
• EKG shows depolarization and repolarization
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Electrocardiography
• EKG is made of waves and segments
• Waves are deflections above or below baseline
• Three waves
1.P wave: depolarization of SA node
2.QRS complex: ventricular depolarization (Atrial
repolarization record is masked by the larger
QRS complex)
3.T wave: ventricular repolarization
• Segments are sections of baseline between waves
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An Electrocardiogram
Figure 20.14b
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Cardiac muscle contraction
• Two types of cardiac muscle cells that are
involved in a normal heartbeat:
• Specialized muscle cells of the conducting
system
• Contractile cells
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Cardiac muscle contraction – conductive cells
• Conductive cells have unstable resting potentials/ pacemaker
potentials
• They constantly depolarized slowly towards AP
• At threshold, Ca2+ channels open
• Ca2+ influx produces the rising phase of the action potential
• Repolarization results from inactivation of Ca2+ channels and
opening of voltage-gated K+ channels
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Cardiac muscle contraction - Contractile Cells
• In cardiac muscle, slow calcium channels remain open
longer (after sodium channels close), prolonging the
depolarization of the cell.
• As long as the action potential is in its plateau and
calcium is entering the myocytes, the myocytes contract.
• These plateaus are more pronounced in the ventricles.
• Cardiac muscle has an absolute refractory period of 250
msec, compared with 1–2 msec in skeletal muscle.
• The cardiac muscle must return completely to resting
potential before it can be contracted again.
• As a result, the heart can not go through tetanus
contraction.
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Action potential in contractile cardiac muscle cells
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Extrinsic Innervation of the Heart
• Heartbeat is modified by the ANS
• Cardiac centers are located in the medulla oblongata
• Cardioacceleratory center innervates SA and AV
nodes, heart muscle, and coronary arteries through
sympathetic neurons
• Cardioinhibitory center inhibits SA and AV nodes
through parasympathetic fibers in the vagus nerves
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Homeostatic Imbalances
•
Defects in the intrinsic conduction system may
result in
1. Arrhythmias: irregular heart rhythms
2. Uncoordinated atrial and ventricular contractions
3. Fibrillation: rapid, irregular contractions; useless
for pumping blood
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Homeostatic Imbalances
• Defective SA node may result in
• Ectopic focus: abnormal pacemaker takes over
• If AV node takes over, there will be a junctional
rhythm (40–60 bpm)
• Defective AV node may result in
• Partial or total heart block
• Few or no impulses from SA node reach the
ventricles
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Heart Sounds
• Two sounds (lub-dup) 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
• Heart murmurs: abnormal heart sounds most often
indicative of valve problems
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Aortic valve sounds heard
in 2nd intercostal space at
right sternal margin
Pulmonary valve
sounds heard in 2nd
intercostal space at left
sternal margin
Mitral valve sounds
heard over heart apex
(in 5th intercostal space)
in line with middle of
clavicle
Tricuspid valve sounds typically
heard in right sternal margin of
5th intercostal space
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Figure 18.19
Cardiodynamics
• Movements and forces generated during cardiac contractions
• End-diastolic volume (EDV) – the amount of blood in each
ventricle at the end of ventricular diastole (before contraction
begins)
• End-systolic volume (ESV) - the amount of blood remains in
each ventricle at the end of ventricular systole
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Cardiodynamics
• Stroke volume (SV) – The amount of blood that leaves the
heart with each beat or ventricular contraction; EDV-ESV=SV
• Not all blood ejected
• Normal Adult 70 ml / beat
• Ejection fraction – The percentage of end-diastole blood
actually ejected with each beat or ventricular contraction.
• Normal adult 55-70% (healthy heart)
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Stroke Volume and Cardiac Output
• Cardiac output (CO) – the amount of blood pumped by
each ventricle in one minute.
• Physiologically, CO is an indication of blood flow through
peripheral tissues
• Cardiac output equals heart rate times stroke volume;
Normal CO: Approximately 4-8 liters/minute
CO
Cardiac output
(ml/min)
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SV
HR
=
Heart rate
(beats/min)
X
Stroke
volume
(ml/beat)
Factors Affecting Cardiac Output
Figure 20.20
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• Effect inotropy – effect on contractility of the heart
• Effect chronotropy – effect on HR
• Effect dromotropy – effect on the conductive velocity
• Sympathetic stimuli has a positive effect (increase) all
• Parasympathetic stimuli has a negative effect (decrease)
all
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Autonomic Nervous System Regulation
• In healthy conditions, parasympathetic effects dominate and slows
the rate of the pacemaker from 80-100 bpm to a 70-80 bpm.
• The binding of Ach to muscarinic receptors (M2) inhibit NE
release (mechanism by which vagal stimulation override
sympathetic stimulation)
• Sympathetic nervous system is activated by emotional or physical
stressors
• Norepinephrine causes the pacemaker to fire more rapidly (and
at the same time increases contractility)
• Parasympathetic nervous system opposes sympathetic effects
• Acetylcholine hyperpolarizes pacemaker cells by opening K+
channels
• The heart at rest exhibits vagal tone (parasympathetic)
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Autonomic Nervous System Regulation
• Atrial (Bainbridge) reflex: a sympathetic reflex
initiated by increased venous return
• Stretch of the atrial walls stimulates the SA node
• Also stimulates atrial stretch receptors activating
sympathetic reflexes
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Effects on SA node
• The effect of the ANS on the heart is by changing the
permeability of the conducting system cells.
• Ach released by the parasympathetic neurons slow the
depolarization rate and extend slightly the repolarization.
• This decreases the HR
• The NE released by the sympathetic neurons binds to beta–1
receptors, leading to the opening of calcium ion channels.
• That increases the depolarization rate and shortens the
repolarization period. Threshold is reached more quickly and
HR increases
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Chemical Regulation of Heart Rate
1. Hormones
•
Epinephrine from adrenal medulla enhances heart
rate and contractility
•
Thyroxine increases heart rate and enhances the
effects of norepinephrine and epinephrine
2. Intra- and extracellular ion concentrations (e.g.,
Ca2+ and K+) must be maintained for normal heart
function
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Homeostatic Imbalances
• Tachycardia: abnormally fast heart rate (>100 bpm)
• If persistent, may lead to fibrillation
• Bradycardia: heart rate slower than 60 bpm
• May result in grossly inadequate blood circulation
• May be desirable result of endurance training
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Factors Affecting Stroke Volume
Figure 20.23
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Regulation of Stroke Volume
• SV = EDV – ESV
• Three main factors affect SV
• Preload
• Contractility
• Afterload
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Regulation of Stroke Volume
• Preload
• The amount of a muscle stretching before it begins to
contract.
• The preload of the heart is determined by the EDV.
• In general, the greater the EDV the larger is the stroke
volume : EDV-ESV=SV
• These relationships is known as the FrankStarling principle/Sterling’s law of the heart :
• The force of cardiac muscle contraction is
proportional to its initial length
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 Preload =  Contractility (to a point)
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Factors Affecting stroke volume - Preload/EDV
• Stroke volume is the difference between the EDV and ESV.
Changes in either one can change the stroke volume and cardiac
output:
• The EDV volume is affected by 2 factors:
• The filling time – duration of ventricular diastole (assuming
venous return is constant)
• depends on HR – the faster the HR the shorter is the
available filing time
• The venous return – amount of blood returning to heart by
the venae cavae or pulmonary veins each minute
• changes in response blood volume (if blood volume
decreases so will venous return), muscle contractions
that press veins or changes in tissue activity.
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Diastolic filling increased
EDV increase (preload increased)
Cardiac muscle stretch increased
Force of contraction increased
Ejection volume increased
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Regulation of Stroke Volume
• Contractility
• Force of ventricular contraction (systole) regardless of
EDV
• Positive inotropic agents increase contractility
• Increased Ca2+ influx due to sympathetic
stimulation
• Hormones (thyroxine and epinephrine)
• Negative inotropic agents decrease contractility
• Increased extracellular K+
• Calcium channel blockers
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Regulation of Stroke Volume
• Afterload
• The amount of tension the ventricle need to produce to open
the semilunar valves and eject blood to arteries
• influenced by arterial pressure.
• The greater is the afterload, the longer is the period of
isovolumetric contraction (ventricles are contracting but
there is no blood flow), the shorter the duration of
ventricular ejection and the larger the ESV – afterload
increase – stroke volume decrease
• Hypertension increases afterload, resulting in increased
ESV and reduced SV
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Congestive Heart Failure (CHF)
• Progressive condition where the CO is so low that blood
circulation is inadequate to meet tissue needs
• Caused by
• Coronary atherosclerosis
• Persistent high blood pressure
• Multiple myocardial infarcts (decreased blood supply
and myocardial cell death)
• Dilated cardiomyopathy (DCM) – heart wall weakens
and can not contract efficiently. Causes are unknown but
sometimes associated with toxins (ex. Chemotherapy),
viral infections, tachycardia and more
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