Transcript Sherwood 9

Chapter 9
Cardiac Physiology
Outline
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Comparison of types of muscle tissue
Circulatory system overview
Anatomy
Electrical activity
Mechanical events
Cardiac output
Coronary circulation
• The next series of slides compares cardiac, skeletal,
smooth muscle cells.
Cardiac muscle
Smooth muscle
Skeletal muscle
Muscle excitation
Muscle excitation
Rise in cytosolic Ca2+
(mostly from
extracellular fluid)
Series of
biochemical events
Phosphorylation of
myosin cross bridges
in thick filament
Binding of actin and
myosin at cross
bridges
Rise in cytosolic Ca2+
(entirely from intracellular
sarcoplasmic reticulum)
Comparison of the
Role of Calcium In
Bringing About
Contraction in
Smooth, Skeletal,
and Cardiac
Muscle
Physical repositioning
of troponin and
tropomyosin
Uncovering of crossbridge binding sites on
actin in thin filament
Binding of actin and
myosin at cross
bridges
Pi
Fig. 8-31, p. 296
Contraction
Contraction
Skeletal
smooth
cardiac
Cardiac Muscle Fibers
• Interconnected by intercalated discs and form functional syncytia
• Within intercalated discs – two kinds of membrane junctions
– Desmosomes
– Gap junctions
• Ap’s
Skeletal Muscle Fiber
Myofibrils
Basal lamina
Sacrolemma
Longitudinal
system
Mitochondria
Transverse
tubule
Nucleus
Intercalated
disc
Myofibril
Opening of
Transverse
tubule
fig 16-8b, pg 487
Smooth Muscle Fiber
Rough
Endoplasmic
reticulum
Glycogen
granules
Nucleus
Mitochondria
Thin filament
Thick filament
Dense
bodies
Plasma
membrane
fig 16-9a, pg 479
Outline
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Comparison of types of muscle tissue
Circulatory system overview
Anatomy
Electrical activity
Mechanical events
Cardiac output
Coronary circulation
Anatomy
Heart
Hollow, muscular organ about
the size of a clenched fist
Positioned between two bony
structures – sternum and
vertebrate
97935
Human heart.
Circulatory System
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Three basic components
– Heart
• Serves as pump that
establishes the pressure
gradient needed for blood to
flow to tissues
– Blood vessels
• Passageways through which
blood is distributed from heart
to all parts of body and back
to heart
– Blood
• Transport medium within
which materials being
transported are dissolved or
suspended
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Pulmonary circulation
– Closed loop of vessels carrying
blood between heart and lungs
Systemic circulation
– Circuit of vessels carrying blood
between heart and other body
systems
Circulatory System
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Heart
Arteries
• Carry blood away from ventricles to tissues
Veins
• Vessels that return blood from tissues to the atria
Septum
– Continuous muscular partition that prevents mixture of blood from the
two sides of heart
Dual pump
– Right and left sides of heart function as two separate pumps
– Divided into right and left halves and has four chambers
Atria
– Upper chambers
– Receive blood returning to heart and transfer it to lower
chamber
Ventricles
– Lower chambers which pump blood from heart
Outline
• Internal Anatomy
– Thoracic cavity, base, apex
– AV and semilunar valves
– endothelium, myocardium, epicardium
– cardiac cells, intercalated disks
– Comparison of cardiac cells to skeletal and
smooth muscle cells
– pericardium
Heart Valves
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Atrioventricular (AV) valves
– Prevent backflow of blood from ventricles into
atria during ventricular emptying
– Right AV valve = tricuspid valve
– Left AV valve = bicuspid valve or mitral valve
– Chordae tendinae
• Fibrous cords which prevent valves from
being everted
• Papillary muscles
Semilunar valves
– Aortic and pulmonary valves
– Lie at juncture where major arteries leave
– ventricles
– Prevented from everting by anatomic structure
– and positioning of cusps
No valves between atria and veins
– Reasons
• Atrial pressures usually are not much
higher than
• venous pressures
• Sites where venae cavae enter atria are
• partially compressed during atrial
contraction
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3 layers
• Consists of three distinct layers
– Endothelium
• Thin inner tissue
• Epithelial tissue which lines entire
circulatory system
– Myocardium
• Middle layer
• Composed of cardiac muscle
• Constitutes bulk of heart wall
– Epicardium
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• Thin external layer which covers the
heart
Pericardium
– the fluid filled sac that surrounds the
heart
Endocardium
Myocardium
Epicardium
Outline
• Electrical activity of the heart
– Autorhymicity
– Pacemaker (function, ions)
– Conductive system (SA, AV, bundle of His,
Purkinje fibers)
– Abnormal rhythms
– Spread of cardiac excitation
– Cardiac cell action potentials
• Characteristics vary by location
Electrical Activity of Heart
• Heart beats rhythmically as result of action potentials it generates by
itself (autorhythmicity)
• Two specialized types of cardiac muscle cells
– Contractile cells
• 99% of cardiac muscle cells, do mechanical work of
pumping,normally do not initiate own action potentials
– Autorhythmic cells
• Do not contract but send electrical signals to the contractile cells,
specialized for initiating and conducting action potentials
responsible for contraction of working cells
Electrical Activity of Heart
• Locations of noncontractile cells capable of autorhymicity
– Sinoatrial node (SA node)
• Specialized region in right atrial wall near opening of superior
vena cava
• Pacemaker of the heart
– Atrioventricular node (AV node)
• Small bundle of specialized cardiac cells located at base of
right atrium near septum
– Bundle of His (atrioventricular bundle)
• Cells originate at AV node and enters interventricular septum
• Divides to form right and left bundle branches which travel
down septum, curve around tip of ventricular chambers,
travel back toward atria along outer walls
– Purkinje fibers
• Small, terminal fibers that extend from bundle of His and
spread throughout ventricular myocardium
Interatrial
pathway
Sinoatrial
(SA) node
Atrioventricular
(AV) node
Right atrium
Left atrium
Internodal
pathway
Left branch
of bundle
of His
Right ventricle
Left ventricle
Right branch
of bundle
of His
Purkinje
fibers
(a) Specialized conduction system of the heart
Fig. 9-8a, p. 312
Electrical Activity of Heart
• Cardiac impulse originates at SA node
• Action potential spreads throughout right and left atria
• Impulse passes from atria into ventricles through AV node
(only point of electrical contact between chambers)
• Action potential briefly delayed at AV node (ensures atrial
contraction precedes ventricular contraction to allow complete
ventricular filling)
• Impulse travels rapidly down interventricular septum by
means of bundle of His
• Impulse rapidly disperses throughout myocardium by means
of Purkinje fibers
• Rest of ventricular cells activated by cell-to-cell spread of
impulse through gap junctions
Pacemaker potential
and
Action potential in autorhythmic cells
• Pacemaker activity - slow depolarization or
drift towards threshold
• Increased inward Na movement
• Decreased outward K movement
• Inward Ca movement
Physiology of pacemaker cells
End of repol opens funny channels
Na channels that open upon hyperpolarization
Fig. 9-7, p. 311
Conduction between
atria and ventricles
• AV nodal delay 100 msec allows
ventricular filling
• Purkinje cell transmission in 30 msec
• Some spreading thru gap junctions
Action potential of cardiac
contractile cell
• Different than nodal pacemaker cell
(conductive cell)
• Rp = -90mv
• K channel subtypes
– Leak channel keeps -90 mv
– Peak potential efflux channels (brief
repol)(fast transient); Cessation of efflux plus
Ca influx creates plateau
– Ordinary k channels repolarize
Electrical Activity of Heart
• Atria contract as single unit followed after
brief delay by a synchronized ventricular
contraction
• Action potentials of cardiac contractile
cells exhibit prolonged positive phase
(plateau) accompanied by prolonged
period of contraction
– Ensures adequate ejection time
– Plateau primarily due to activation of slow Ltype Ca2+ channels
Electrical Activity of Heart
• Ca2+ entry through L-type channels in T tubules triggers
larger release of Ca2+ from sarcoplasmic reticulum
– Ca2+ induced Ca2+ release leads to cross-bridge cycling and
contraction
• Because long refractory period occurs in conjunction
with prolonged plateau phase, summation and tetanus of
cardiac muscle is impossible
– Ensures alternate periods of contraction and relaxation which
are essential for pumping blood
– Refractory= unresponsive to stimulus
Relationship of an Action Potential and the Refractory Period to the
Duration of the Contractile Response in Cardiac Muscle
Physiology of contractile cell
Interatrial
pathway
SA node
AV node
Right atrium
Left atrium
Interatrial
pathway
Bundle
of His
Electrically
nonconductive
fibrous tissue
Left ventricle
Right ventricle
Purkinje
fibers
(b) Spread of cardiac excitation
Fig. 9-8b, p. 312
Coordination of noncontractile and contractile cells
SA node
pacemaker
Atrial muscle
Atrioventricular
Bundle branch
Purkinje fibers
Ventricular
muscle
Milliseconds
fig. 18-13; pg: 568
Electrocardiogram (ECG)
• Record of overall spread of electrical activity through heart
• Represents
– Recording part of electrical activity induced in body fluids
by cardiac impulse that reaches body surface
• Not direct recording of actual electrical activity of heart
– Recording of overall spread of activity throughout heart
during depolarization and repolarization
• Not a recording of a single action potential in a single cell at a
single point in time
– Comparisons in voltage detected by electrodes at two
different points on body surface, not the actual potential
• Does not record potential at all when ventricular muscle is
either completely depolarized or completely repolarized
SA node
fires
TP interval =
Time during which
ventricles are
relaxing and filling
Recorded potential
P wave =
Atrial depolarization
R
200 msec
T
P
Q
PR
segment
P
PR segment =
AV nodal delay
S
ST
segment
TP
interval
T wave =
Ventricular
repolarization
ST segment =
Time during which
ventricles are contracting
and emptying
QRS complex =
Ventricular depolarization
atria repolarizing
simultaneously)
Fig. 9-14, p. 320
Credit: © Mediscan/Visuals Unlimited
Normal ECG.
3202
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Rhythm
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Abnormalities in
Rhythm and rate
Regularity or spacing of ECG waves
Arrhythmia
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Variation from normal rhythm and
sequence of excitation of the heart
• Atrial flutter (200-300 BPM)
• Atrial fibrillation
• Ventricular fibrillation
• Heart block
Tachycardia >100 beats per minute
Bradycardia < 60 beats per minute
Damage of the heart muscle
– Myocardial ischemia
• Inadequate delivery of oxygenated blood to heart
tissue
– Necrosis
• Death of heart muscle cells
– Acute myocardial infarction (heart attack)
• Occurs when blood vessel supplying area of
heart becomes blocked or ruptured
Outline
• Mechanical events
– Systole, diastole
– animation (volumes, pressures, sounds and EKG)
Specialized Conduction System of Heart
Cardiac Output
• Volume of blood ejected by each ventricle each
minute
• Determined by
heart rate times
stroke volume
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Heart rate is varied
by altering balance of
parasympathetic and
sympathetic influence
on SA node:
– Parasympathetic
stimulation slows
heart rate
– Sympathetic
stimulation
speeds it up
Fig. 9-20a, p. 329
Cardiac Output
• Stroke volume
– Determined by extent of venous return and by
sympathetic activity
– Influenced by two types of controls
• Intrinsic control
• Extrinsic control
– Both factors increase stroke volume by increasing
strength of heart contraction
Frank-Starling Law of the Heart
• States that heart normally pumps out during systole
the volume of blood returned to it during diastole
End-diastolic volume
175 ml
End-diastolic volume
135 ml
Stroke volume
70 ml
End-diastolic volume
135 ml
Stroke volume
100 ml
Stroke volume
140 ml
End-systolic volume
65 ml
End-systolic volume
35 ml
(a) Normal stroke
volume
(b) Stroke volume
during sympathetic
stimulation
End-systolic volume
35 ml
(c) Stroke volume with
combination of
sympathetic stimulation
and increased enddiastolic volume
Fig. 9-23, p. 331
Coronary circulation
Nourishing the Heart Muscle
• Muscle is supplied with oxygen and nutrients by
blood delivered to it by coronary circulation, not from
blood within heart chambers
• Heart receives most of its own blood supply that
occurs during diastole
– During systole, coronary vessels are compressed
by contracting heart muscle
• Coronary blood flow normally varies to keep pace
with cardiac oxygen needs
Coronary Artery Disease (CAD)
• Pathological changes within coronary artery walls
that diminish blood flow through the vessels
• Leading cause of death in United States
• Can cause myocardial ischemia and possibly lead to
acute myocardial infarction
– Three mechanisms
• Profound vascular spasm of coronary arteries
• Formation of atherosclerotic plaques
• Thromboembolism
Normal blood
vessel wall
Collagen-rich
smooth muscle
cap of plaque
Plaque
Lipid-rich core
of plaque
Endothelium
Fig. 9-29, p. 328
Fig. 9-30, p. 330
Area of cardiac muscle
deprived of blood supply
if coronary vessel is
blocked at point A:
Area of cardiac muscle
deprived of blood supply
if coronary vessel is
blocked at point B:
A
Right coronary
artery
Left coronary
artery
Left ventricle
Right ventricle
B
Fig. 9-31, p. 339
Table 9-4 p339