The Heart
Chambers of the Heart
Cardiac Cycle
Ventricular systole
- isovolumic contraction
- ejection
Ventricular diastole
- isovolumic relaxation
- rapid filling
- atrial contraction
1) Isovolumic
Ventricular Contraction
3) Isovolumic
Ventricular Relaxation
2) Ventricular Ejection
4) Ventricular Filling
5) Atrial Contraction
Can the heart beat by itself ?
Autorhythm
The heart can beat on its own without the need
for exogenous commands.
Conclusion ?
The heart generates electricity.
Motor nerve
Skeletal muscle
TERMINOLOGY
Excitation
- definition: generation of action potentials
- different from contraction
Contraction
- definition: shortening of muscle cells
- triggered by excitation
Excitation-Contraction coupling
Excitation
(Action Potentials)
++
[ Ca
]i
Contraction
(shortening)
Sequence of excitation
Sinus-Atrial node (SA node)
Atria
Atrial-ventricular node (AV node)
Ventricles
Original Impulses from S-A Node
The electrical impulses are normally generated by a
group of specialized pacemaker cells at sinoatrial (SA)
node.
SA node
- located in the
right atrial wall,
just inferior to
the entrance of
the superior
vena cava.
Conduction of Electrical Impulses in the Heart
Conduction of Action Potentials from Cell to Cell
through gap junctions in intercalated discs
(electrical synapses)
Conduction in Atria
The electrical impulses from SA node spread
through the entire right and left atrial muscle
mass, triggering contraction of the right and
left atrium.
Delay at A-V Node
- The impulses from S-A
atrioventricular (A-V) node.
node
travel
to
- A-V node is located in lower end of the interatrial
septum near the tricuspid valve.
A-V node
Delay at A-V Node
- Conduction speed in A-V node is slow (delay).
- This delay allows time for the
atria to finish contraction and
empty their contents into the
ventricles before ventricles start to
contract.
- A-V node is the only normal
route that impulses from SA
node are transmitted into
ventricles.
From AV node to Ventricles
His bundle
- left branch (anterior/posterior division)
- right branch
His bundle
Rapid Conduction in Ventricles
After the delay at A-V node, the impulses rapidly spread to
the ventricles via specialized fibers, Purkinje fibers.
1) Purkinje fibers
- located in the
subendocardial layer
- fastest conduction (4 m/s)
2) Ordinary ventricular
myocardial cells
able to conduct AP at a
slower speed
Rapid conduction in the ventricles
simultaneous excitation of the ventricles
functional syncytium
NNote:
- Each electrical impulse can trigger cardiac
muscle contraction normally only once.
- A normal heart generates 60 to 100 impulses in 1
minute at resting state.
1
1
Properties of Cardiac Muscle
Excitation of the heart is triggered by
electrical impulse rather than neural transmitters.
Contraction of the heart is triggered by
elevation of intracellular calcium influx.
Excitation
(Action Potentials)
[ Ca
++
]i
Contraction
(shortening)
Properties of Cardiac Muscle
- Myocytes depend heavily on oxygen and blood
supply.
- Not fatigue
- Excitability Cycle
The myocytes have Long refractory
period during which they do not respond
to any electrical impulses.
RRole of a Long Refractory Period – 1
prevent ventricles from
contracting at too high rates so that enough
time is allowed for refill of the ventricles
Role of Long refractory period - 2
Prevent retrograde excitation
ELECTROCARDIOGRAPHY
(ECG)
EELECTROCARDIOGRAPHY
((ECG)
the recording of electrical activities of the heart via
electrodes placed on body surface.
QRS: potential changes during depolarization
Applications of ECG
1) measure automaticity
HR, rhythmicity, pacemaker
2) measure conductivity
pathway, reentry, block
3) reveal hypertrophy
4) reveal ischemic damages
location, size, and progress
Waves and Intervals of ECG
P wave:
atrial depolarization
QRS complex:
ventricular depolarization
T wave:
ventricular repolarization
PR Interval
Disorders of the Cardiac Conduction
System ---- Arrhythmias
- refers to abnormal initiation or conduction
of electrical impulses in the heart.
- caused by ischemia, fibrosis, inflammation,
or drugs.
Bradycardia
slow heart rate ( < 60 beats/min)
Tachycardia
fast heart rate ( > 100 beats/min)
Atrial or Ventricular Flutter and Fibrillation
- contract
uncoordinatedly and
extremely rapidly.
- Ventricular fibrillation
is lethal.
Premature contraction
is when the heart beat is triggered by
ectopic pacemakers (cells other than SA node).
Conduction Block
Artificial Pacemaker
Application:
sinus abnormality,
complete AV or ventricular
block
Function:
- generate electric pulses
- sensing
- antitachyarrhythmia
Heart Sounds
Four heart sounds can be recorded via
phonocardiography, but normally only two,
the first and the second heart sounds, are
audible through a stethoscope.
First heart sound:
- occurs when the
atrioventricular (AV) valves
close at the beginning of
ventricular contraction.
- generated by the vibration of
the blood and the ventricular
wall
- is louder, longer, more
resonant than the second heart
sound.
Second heart sound
- occurs when aortic and
pulmonary semilunar
valves close at the
beginning of ventricular
dilation
- generated by the vibration
of the blood and the aorta
- Aortic valve closes slightly
before pulmonary valve.
Heart Murmur
- abnormal heart sound
- occur in valvular diseases and
septal defects
Two Basic Types of Valvular Diseases
1) valvular stenosis, a
narrowing of the valve
2) valvular insufficiency
(incompetence). A valve is
unable to close fully; so
there is some backflow
(regurgitation) of blood.
MECHANICAL PROPERTIES OF THE HEART
CONTENT
Heart Rate
Stroke volume
Cardiac Output (CO)
Ejection Fraction
Preload
Afterload
Contractility
Frank-Starling Mechanism
Factors on Cardiac Output
Heart Rate
the number of heart
beats in 1 minute.
Normal value: 60100/min
Stroke volume
the volume of blood
pumped out by each
ventricle per each
contraction.
SV
Cardiac Output (CO)
the amount of blood pumped out by each ventricle in
1 minute.
Cardiac output = stroke volume x heart rate
Example:
70
ml
70 ml x 75 beat/min = 5,250 ml/min
75 beat/min
Ejection Fraction
= stroke volume end-diastolic ventricular volume
70 ml  130 ml
= 54%
SV =
70 ml
130 ml
End of diastole
60 ml
End of systole
Ejection Fraction
increases during exercise
120 ml  133 ml = 90%
SV =
120 ml
133 ml
End of diastole
End of systole
Preload
the force that stretches the muscle before
contraction.
Afterload
the force that stretches muscle during
contraction.
preload
afterload
Preload to ventricles = ventricular end diastolic pressure
- the degree of stretch of the ventricular muscle cells
just before they contract.
- determined by ventricular filling.
Afterload to left ventricle: aortic arterial pressure
Afterload to right ventricle: pulmonary arterial pressure
Afterload
to the left
ventricle
is greater
than that
to the
right
ventricle.
Aortic arterial pressure
Contractility
- the intrinsic strength of cardiac muscles.
Factors on Cardiac Output
1) Preload:
2) Afterload:
3) Contractility:
4) Heart Rate:
Factors on Cardiac Output
1) Preload:
 Preload   cardiac output
(Starling-Frank Mechanism)
Factors on Cardiac Output
More out
1) Preload:
 Preload   cardiac output
(Starling-Frank Mechanism)
More in
Factors on Cardiac Output
1) Preload:
2) Afterload:
 afterload   CO
R
Factors on Cardiac Output
1) Preload:
2) Afterload:
3) Contractility:
 contractility   CO
Factors on Cardiac Output
1) Preload:
2) Afterload:
3) Contractility:
4) Heart Rate:
dual effects
CO = Heart Rate x Stroke Volume
Factors on Cardiac Output
Stoke Volume
less out
1) Preload:
2) Afterload:
3) Contractility:
less in
4) Heart Rate:
Heart Rate
dual effects
CO = Heart Rate x Stroke Volume
300%
400%
REGULATION OF THE HEART FUNCTION
Regulation of the Cardiac Function
1) Nervous control
•
Sympathetic control
•
Parasympathetic control
•
Higher centers
•
Reflexes
2) Hormonal Control
3) Autoregulation
4) Other factors
Regulation of the Cardiac Function
1) Nervous control
•
Sympathetic control
•
Parasympathetic
control
Sympathetic Nervous System
- controls all components of the heart.
- release Norepinephrine (NE).
- increases heart rate (positive chronotropic) and
contractility (positive inotropic).
1
Cell
Parasympathetic Nervous System (PNS)
- controls SA node and AV node.
- releases Acetylcholine (Ach).
- decreases heart rate (negative chronotropic).
- prolongs delay at AV node.
- has little effect on contractility.
m
Cell
Higher Centers of
Autonomic Nervous
System
- Medulla
Oblongata
- Hypothalamus,
Thalamus, Cerebral
cortex
Centers in Medulla Oblongata
Sympathetic center:
distinct accelerator and augmentor
Parasympathetic center:
Nucleus vagus and nucleus ambiguus
Hypothalamus, Thalamus, Cerebral cortex
Involved in the cardiac response to environmental
temperature changes, exercise, or during
excitement, anxiety, and other emotional states
Neural Control via Reflexes
Baroreceptors
1) Baroreceptor Reflex
- stimulated by increase in arterial pressure (stretch)
- Effect: negative chronotropic and inotropic
- regulate the heart when BP increases or drops
- involved in short term regulation of BP
2) Chemoreceptor Reflex
Chemoreceptors
Chemoreceptors
Chemoreceptors
2) Chemoreceptor Reflex
- stimulated by oxygen, pH, or CO2
- overall effect: positive choronotropic and inotropic.
- less important in regulating cardiac function
3) Proprioceptor Reflex
- Stimulated by muscle and joint movement
- Effects: increase heart rate during exercise
Regulation by Hormones
Epinephrine
- released from adrenal
gland.
- increases heart rate
and contractility.
Thyroxin
- released from thyroid
gland.
- increases heart rate.
Autoregulation of the Heart
Stroke volume is autoregulated by ventricular
filling (Frank-Starling law).
More in
SV
More out
4) Other Factors
- Blood level of ionic calcium, sodium, and
potassium
Hypercalcemia (high plasma Ca++):
positive inotropic
Hypernatremia (high plasma Na+):
negative chronotropic
Hyperkalemia (high plasma K+):
negative chronotropic
used in lethal injection
- Age, gender, exercise, and body temperature
Blood Supply to Cardiac Muscles
Can cardiac muscles get nutrients from the
blood in heart chambers?
The cardiac muscles get nutrients from
coronary circulation.
Anterior view
Posterior view
Coronary arterial anastomosis
endocardium
epicardium
LV
RV
Coronary venous blood is emptied into the right
atrium through cardiac veins and coronary sinus.
Posterior view
coronary sinus
Blockade of coronary artery causes myocardial
infarction, or heart attack.
endocardium
epicardium
LV
RV
Coronary Atherosclerosis
Typical lesion of Coronary Atherosclerosis
dull white and
slightly elevated
fibrous plaque
(atheroma) on
coronary arterial
lumen.
Histology of the plaque
Ccomposed of lipid,
smooth muscle,
macrophages, and
connective tissues.
cause stenosis of
coronary arteries
 occlude arterial
lumen when combined
with internal
hemorrhage,
thrombosis, and
arterial spasm
 occur often at arterial branching points
Surgical Therapies
1)
2) Coronary angioplasty
3) Stenting