The Heart
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Functions of the Heart
1.
2.
3.
4.
Generate blood pressure
Routing blood
Ensures one-way blood flow
Regulating blood supply
Anatomy of the Heart
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Review pages 670 to 676
Pay particular attention to heart chambers and
valves. (pg. 675-676).
Cardiac Muscle
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Similar to skeletal muscle.
ATP is used for energy to fuel contraction.
Rich in mitochondria.
Extensive capillary network providing O2.
Cardiac Muscle
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Specialized plasma membrane structures
called desmosomes hold cells together.
Areas of low resistance between cells called
gap junctions allow action potentials to move
from one cell to the next.
Conducting System
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Two nodes in the cardiac muscle.
Located in the right atrium.
– Sinoatrial (SA) node.
– Atrioventricular (AV) node.
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AV node gives rise to the atrioventricular (AV)
bundle.
AV bundle divides to form right and left bundle
branches.
Conducting System
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Right and left bundle branches terminate in
Purkinje fibers.
Cardiac muscle cells have the capacity to
generate spontaneous action potentials.
SA node sets the cardiac rhythm (pacemaker).
Conducting System
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Once action potentials are initiated at SA
node, they spread across the atrium.
The action potentials also travel to the AV
node on a pathway that allows a greater
velocity.
Therefore, the action potential reaches the AV
node before they reach the remainder of the
atrium muscle.
Conducting System
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At rest, it takes approx. 0.04 second for action
potentials to travel from the SA node to the AV
node.
Action potentials slow down considerably at
the AV node.
It takes 0.11 second for the action potentials
to travel through the AV node.
Conducting System
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After the action potentials pass through the AV
node the conduction velocity increases.
Electrical Properties
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Cardiac muscle cells have a resting
membrane potential that depends on:
– Low permeability to Na+ and Ca2+
– Higher permeability to K+
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When the cardiac muscle cell is depolarized to
its threshold, an action potential will result.
Action Potentials
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Action potentials in the cardiac muscle are
similar to what we discussed earlier.
Cardiac muscle action potentials last longer
than those in skeletal muscle.
Action Potentials
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Cardiac muscle action potentials have a:
– Rapid depolarization phase.
– Rapid, partial early repolarization phase.
– Prolonged period of slow repolarization (plateau
phase).
– Rapid final repolarization phase.
Autorhythmicity of Cardiac Muscle
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The heart is autorhythmic because it can
stimulate itself to contract at regular intervals.
In SA node , pacemaker cells generate action
potentials.
These action potentials are generated due to
a spontaneous local potential called a
prepotential.
Autorhythmicity of Cardiac Muscle
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Some cardiac cells can generate their own
spontaneous action potential (ectopic focus).
Ectopic foci can result if the:
– SA node doesn’t function properly
– Blockage of conducting pathways
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However, the rhythm set by the SA node is
more rapid and produces a heart rate of 70-80
bpm.
Refractory Period
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Absolute refractory period
Relative refractory period
Due to the plateau phase and the longer
repolarization period, the refractory period is
longer.
Electrocardiogram
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Action potentials moving through the cardiac
muscle produces electrical currents that can
be measured on the surface of the body.
These currents are measured by electrodes
attached to the surface of the body producing
an electrocardiogram (ECG).
Electrocardiogram
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The ECG is a diagnostic tool that can be used
to determine:
– Abnormal heart rates or rhythms
– Abnormal conduction pathways
– Hypertrophy/atrophy of portions of the heart
Electrocardiogram
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Normal ECG consists of a P wave, QRS
complex, and a T wave.
The time between the beginning of the P wave
and the beginning of the QRS complex is the
PR interval.
The time from the beginning of the QRS
complex to the end of the T wave is the QT
interval.
Arrhythmias
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Arrhythmias are abnormal heart rhythms.
Caused when:
– the heart’s natural pacemaker develops an
abnormal rate or rhythm;
– the normal conduction pathway is interrupted;
– another part of the heart takes over as the
pacemaker.
Arrhythmias
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Slow heartbeat (bradycardia)
– Can cause fatigue, dizziness, lightheadedness,
fainting, or near-fainting spells.
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Rapid heartbeat (tachycardia)
– Can produce rapid heart action, dizziness,
lightheadedness, fainting, or near-fainting spells.
Fibrillation
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Atrial fibrillation:
– Atria quiver instead of beating correctly.
– Blood isn’t pumped out completely.
– Blood may pool and form clots which could lodge
in the brain and produce a stroke.
Fibrillation
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Ventricular fibrillation:
– Ventricles contract in a rapid, unsynchronized,
uncoordinated fashion.
– Little or no blood is pumped from the heart.
Heart Block
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The signal from the atria to the ventricles is impaired
or isn’t transmitted.
Classified by level of impairment:
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First-degree = electrical impulse moves through AV node
more slowly than normal
(> 0.20 sec).
Second-degree = some signals from atria don’t reach the
ventricles (“dropped beats”)
Third-degree = complete AV node block resulting in
ventricles setting their own rhythm.
Cardiac Cycle
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The heart is actually two pumps; a right half
and a left half.
Cardiac cycle refers to the repetitive pumping
process that starts with the beginning of one
contraction and ends at the beginning of the
next contraction.
A normal cardiac cycle lasts 0.7 – 0.8 second.
Cardiac Cycle
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Systole = contract
Diastole = dilate (relax)
We will refer to these terms with respect to the
ventricles.
Cardiac Cycle
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Five phases in the cardiac cycle.
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Systole: Isovolumetric ventricular contraction.
Systole: Ventricular ejection.
Diastole: Isovolumetric ventricular relaxation.
Diastole: Passive ventricular filling.
Diastole: Active ventricular filling.
Isovolumetric Ventricular Contraction
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Ventricles contract.
Pressure rapidly increases.
All valves remain closed – no blood ejected.
Ventricular volume remains constant.
Ventricular Ejection
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Ventricles continue to contract.
Pressure continues to increase.
Pressure in ventricle > pressure in aorta &
pulmonary artery (~80 mmHg).
Aortic & pulmonary valves open.
Pressure peaks at ~120 mmHg.
Blood ejection.
Isovolumetric Ventricular Relaxation
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Ventricles relax after contraction.
Pressure rapidly decreases.
Aortic & pulmonary valves close.
Volume remains constant.
Passive Ventricular Filling
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Atrial pressure exceeds ventricular pressure.
AV valves open.
Blood flows from atria into ventricles.
Accounts for approx. 70% of ventricular filling.
Most filling occurs during first 1/3 of diastole.
Active Ventricular Filling
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Depolarization of SA node generates action
potentials that spread across atria.
Atria contract during last 1/3 of diastole.
Final volume of blood from atria fills during
atrial contraction.
Final volume in ventricle = EDV
Heart Sounds
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LUBB-DUPP
LUBB = closure of the AV valves (beginning of
systole).
DUPP = closure of the pulmonary & aortic
valves.
Mean Arterial Blood Pressure
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MAP is the average blood pressure between
the systolic and diastolic pressure in the aorta.
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MAP  Q x PR
Cardiac output (Q) = HR x SV
Stroke volume (SV) is equal to approximately
70 ml. (EDV – ESV).
Stroke Volume
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SV can be increased by increasing EDV or
decreasing ESV.
This occurs during exercise for example.
EDV increases due to increased venous
return.
ESV decreases because the heart contracts
more forcefully.
Regulation of the Heart
• Intrinsic vs. Extrinsic Regulation.
– Intrinsic
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Preload
Starling’s law of the heart
Afterload
– Extrinsic
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Parasympathetic
Sympathetic
Hormonal
Dynamics of Blood Circulation
1.
2.
3.
4.
5.
6.
Laminar & Turbulent Flow
Blood Pressure
Blood Flow
Poiseuille’s Law
Viscosity
Compliance
1. Laminar & Turbulent Flow
• Laminar flow produces the least
resistance.
• Turbulent flow occurs when laminar flow
is interrupted.
2. Blood Pressure
• Measure of the force that blood exerts
against the walls of blood vessels.
• Measured in mmHg.
• More on blood pressure in the lab.
3. Blood Flow
• Measure of the rate that blood flows
through vessels.
• Measured in liters or milliliters per
minute.
3. Blood Flow
• Blood flow is directly proportional to the
pressure difference in that vessel.
• Blood flow is inversely proportional to the
resistance in the blood vessel.
Flow = (P1 – P2) / R
4. Poiseuille’s Law
• Describes the factors that affect
resistance to blood flow.
Flow = π (P1 – P2) / 8vl / r
Flow = (P1 – P2) r
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4
5. Viscosity
• Measure of the resistance of a liquid to
flow.
• The greater the viscosity, the greater the
pressure to force the fluid to flow.
• The viscosity of the blood is greatly
affected by it’s hematocrit.
6. Compliance
• Compliance = “stretchability”.
• Venous compliance is approx. 24 times
greater than arterial compliance.
• Veins therefore acts as a storage area
(reservoir) for blood
(64% of total blood volume).
Control of Blood Flow in Tissues
• In most tissues, blood flow is
proportional to the metabolic needs of
the tissue.
• Flow is met by dilation of metarterioles
and relaxation of the precapillary
sphincters.
• Blood flow can increase 7-8 times.
Control of Blood Flow in Tissues
• Vasodilator substances are produced as
the rate of metabolism increases.
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CO2
Lactic acid
Hydrogen ions
Etc.
Control of Blood Flow in Tissues
• Nervous & Hormonal Regulation of Local
Circulation.
– Autonomic regulation can function rapidly.
– Sympathetic motor fibers innervate all blood
vessels except capillaries, precapillary
sphincters, and metarterioles.
– Controlled by the vasomotor area in lower
pons and upper medulla oblongata.
Control of Blood Flow in Tissues
• Nervous & Hormonal Regulation of Local
Circulation.
– Areas throughout the pons, midbrain and
diencephalon can stimulate or inhibit the
vasomotor center.
Control of Blood Flow in Tissues
• Nervous & Hormonal Regulation of Local
Circulation.
– Neurotransmitter = norepinephrine
– Binds to α-adrenergic receptors to cause
vasoconstriction.
Control of Blood Flow in Tissues
• Nervous & Hormonal Regulation of Local
Circulation.
– Same effect for the hormones epinephrine
and norepinephrine from adrenal medulla.
– These hormones usually cause
vasoconstriction, but in tissues such as
skeletal muscle, epinephrine binds to
β-receptors and cause vessels to dilate.
Regulation of Mean Arterial Pressure
• MAP = diastolic + 1/3(pulse pressure)
• MAP = Q X PR
• MAP = HR X SV X PR
Regulation of Mean Arterial Pressure
• Short-term Regulation
– Baroreceptor Reflex
• Baroreceptors are receptors that are sensitive
to stretch.
• Most numerous in carotid artery and aortic arch.
Regulation of Mean Arterial Pressure
• Short-term Regulation
– Chemoreceptor Reflex
• Carotid bodies and aortic bodies.
• Stimulated by decreases in oxygen availability,
increases in carbon dioxide & hydrogen ion
concentration.
• Stimulation results in vasoconstriction.
Regulation of Mean Arterial Pressure
• Long-term Regulation
– Renin-Angiotensin-Aldosterone System