Transcript chapter 14 Cardiac B

Heart activity
• Modulation of autorhythmic cells
• Electrical activity co-ordinates heart
contraction
• Pacemakers
• Electrocardiogram shows heart electrical
activity
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Modulation of autorhythmic cells
• NE (sympathetic) and E (adrenal
hormone)
• Autorhythmic cells have beta1 receptors
• Cyclic AMP levels increase
• Properties of If and Ca++ channels altered
• More rapid Na+ and Ca++ entry
• Rapid action potential
• Rapid contractions
Modulation of autorhythmic cells
• Parasympathetic, acetyl choline
• Muscarinic receptors
• K+ channels open mb hyperpolarizes
cell less excitable
• Ca++ channel less likely to open slower
depolarization  cell is less excitable
Electrical activity in the heart
Heart muscular activity
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autorhythmic cells.
Conductive system of the heart
The ECG
Muscular activity
– The five phases of the heart cycle.
The heart’s main pacemaker is in the sinoatrial node (SA node)
where a group of autorhythmic cells are located at the junction of the
vena cava and the right atrium
The conductive
system of the heart
consists of noncontractile
autorhythmic cells
Action potentials spread across atria.
Action potentials encounter fibrous
Tissue at the junction of the atria and
Ventricles.
Action potential reach the ventricles
Through the AV node, then spread
Rapidly down the bundle of His.
Prukinje fibers rapidly transmit
Impulses up the ventricle
All contractile cells at apex
Contract simultaneously
Why does the AV node delay action
potentials?
• This allows the atria to complete
contraction and allows the ventricles to fill
before the ventricles contract
Autorhythmic cells
• All cells of the conducting fibers are
autorhythmic
• The cells of the SA node set the heart rate
because their rhythm is fastest.
• They set the pace.
• If the SA node is damaged, the other
pacemakers still function, the pace lowers.
The electrocardiogram shows the
electrical activity of the heart.
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ECG
Electrodes placed on the skin
On arms and leg
ECG shows summated electrical activity
during heart activity
• Indirectly shows contraction and relaxation
of atria and ventricles
Einthoven’s triangle.
Location of electrode placement
For ECG
The electrocardiogram. Know the points.
ECG
• P wave, atria depolarize
• QRS complex, wave of ventricular
depolarization
• T wave, ventricles repolarize
The heart cycle
• Period from the beginning of one heart
beat to the beginning of the next heart
beat
• Two phases:
– Diastole, period of cardiac muscle relaxation
– Systole, period of cardiac muscle contraction
• The atria and ventricles do not contract
and relax at the same time.
5 phases of the heart cycle
• Heart at rest (atrial and ventricular
diastole)
• Completion of ventricular filling (atrial
systole)
• Early ventricular contraction (first heart
sound)
• The heart pumps (ventricular ejection)
• Ventricular relaxation (second heart
sound)
Heart activity
• Pressure/volume curves represent one cardiac cycle
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Stroke volume is the volume of blood pumped by
one ventricle in one contraction
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Cardiac output is a measure of cardiac
performance
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Heart rate is varied by autonomic neurons and
catecholamines
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Multiple factors influence stroke volume
The heart cycle
• Period from the beginning of one heart
beat to the beginning of the next heart
beat
• Two phases:
– Diastole, period of cardiac muscle relaxation
– Systole, period of cardiac muscle contraction
• The atria and ventricles do not contract
and relax at the same time.
5 phases of the heart cycle
1. Heart at rest (atrial and ventricular
diastole)
2. Completion of ventricular filling (atrial
systole)
3. Early ventricular contraction (first heart
sound)
4. The heart pumps (ventricular ejection)
5. Ventricular relaxation (second heart
sound)
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Heart at rest (atrial and ventricular
diastole)
Atria and ventricles are relaxing
blood flows into the atria from veins
AV valves are open
Blood flows into the ventricles from the
atria
• Relaxed ventricles accept blood
2. Completion of ventricular filling (atrial systole)
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Depolarization from the SA node
Contraction of atria
Blood pushed into the ventricles
Pressure increase accompanies
contraction
• Increase in pressure pushes some blood
back to the veins
3. Early ventricular contraction (first heart sound)
• Depolarization to AV node, down bundle of
His, up Purkinje fibers
• Ventricular systole begins at apex
• Blood pushing up on AV pushes them shut
• Blood does not flow back to atria
• First heart sound when AV valves close
(lub)
3. Early ventricular contraction
(first heart sound)
• The semilunar valves are also shut
• Blood stays in the ventricle while it
contracts
• High pressure on the heart walls during
this contraction
–  ISOMETRIC CONTRATION
3. Early ventricular contraction (first heart sound)
• Atria begin to repolarize and relax
Atrial pressure falls below venous
pressure
Blood flows from veins to atria
 Blood stays in atria because the AV
valves are closed
4. The heart pumps (ventricular ejection)
• Ventricles contract
Semilunar valves open
Ventricular blood is pushed into the
arteries
5. Ventricular relaxation (second heart sound)
Ventricular pressure falls
Blood starts to flow from arteries into
ventricles
This backflow shuts the semilunar valves
(dup of lub-dup)
Ventricles become closed
AV valves open when ventricular pressure
is lower than atrial pressure
Heart activity
• Pressure/volume curves represent one cardiac cycle
•
Stroke volume is the volume of blood pumped by
one ventricle in one contraction
•
Cardiac output is a measure of cardiac
performance
•
Heart rate is varied by autonomic neurons and
catecholamines
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Multiple factors influence stroke volume
End Diastole Volume (EDV)
• Ventricles are maximally filled at the end of
ventricular relaxation (diastole)
• When heart rate is very high, the ventricles
may not have enough time to fill as much
as when the heart rate is slow
End-systole volume (ESV)
• The amount of blood left in the heart at the
end of each contraction
Pressure-volume curves
Match the cardiac cycle.
Left ventricular pressure-volume changes
during one cardiac cycle.
Wiggers
Diagram
Wed. Nov. 30
• Stroke volume
• Cardiac output
• Heart rate is varied by autonomic neurons and
catecholamines
• Factors influencing stroke volume
• Length-tension relationships and Starling’s Law of
the heart
• Stroke Volume and venous return
• Control of contractility
Stroke volume
• Volume of blood pumped out by one
ventricle in one contraction
• Volume of blood before contraction minus
volume of blood after contraction is the
stroke volume.
Stroke Volume
• EDV - ESV = Stroke Volume
• 135 - 65 = 70 ml for normal stroke volume.
Cardiac Output
• A measure of cardiac performance
• The volume of blood pumped out of the
ventricle per unit time indicates the blood
(oxygen) is available to flow into tissues.
Cardiac Output
• Cardiac Output = Heart rate X stroke vol.
• CO = 72 beats/min x 70 ml/beat
• CO = 5040 mL/min (5 L/min)
• This is at rest.
Cardiac Output
• At rest around 5 L/minute
• During exercise up to 35 L/minute
• How does CO increase? (CO = SV x HR)
Effect of autonomic neurons and
catecholamines.
• Effect on autorhythmic cells in the SA
node.
• Sympathetic and parasympathetic division
of the autonomic nervous system have
antagonistic effects.
• Parasympathetic effect slows heart rate.
• Sympathetic effect speeds up heart rate.
• Tonic control of heart is dominated by the
parasympathetic branch.
Increase heart rate
Decrease parasympathetic influence on SA
autorhythmic cells. --> Autorhythmic cells
resume intrinsic rate of depolarization.
To increase heart rate above intrinsic autorhythmic
rate, increase sympathetic input.
Influence on action potential
conduction.
• Acetyl choline (parasympathetic) slows
down neural activity through the AV node.
• Epinephrine and norepinephrine
(catecholamines) speed up neural activity
through the AV node.
Stroke volume influences
• The force of contraction.
• Contractility: increasing sarcomere length
makes cardiac muscle more sensitive to
calcium.
• Link between muscle length and
contractility.
Length-tension relationships
• Tension created during a contraction
increases as sarcomere length increases
up to an optimal length.
• Stroke volume increases with tension in
the ventricular wall.
Starling’s Law of the Heart
• Isolated heart/lung prep pumps all blood
returned to it.
• (nervous or hormonal influence absent)
Starling Curve - relationship between
stretch and force in the intact heart.
Frank-Starling Law of the Heart
• Within physiological limits, the heart
pumps all of the blood that returns to it.
• The stroke volume (amount of blood
ejected from the ventricle per contraction)
is proportional to force (amount of blood in
the ventricle).
Frank-Starling Law
• The more blood there is in the ventricle at
the beginning of a contraction (EDV), the
greater the stroke volume.
• The venous return determines the EDV
(myocardial stretch, the pre-load).
Venous return is affected by:
• Compression of veins returning blood to
the heart.
• Pressure changes during breathing
• Sympathetic innervation of veins.
Pressure changes during breathing
• Enhanced venous return during
inspiration.
• Low pressure in thorax during inhalation
draws blood into vena cava from
abdominal veins.
Control of contractility.
• Contractility increases as the calcium
available for contraction increases.
• Catecholamines (NE, E) increase calcium
entry and calcium sequestering.