Download Chapter 14 Heart: Cardiovascular Physiology Part 2 For Friday, start

Chapter 14
Heart: Cardiovascular Physiology
Part 2
For Friday, start with slide #42
Exam 3 will be on Monday November 21
Will cover chapters 11, 12, 13, 14
May cover more, depends on how far we get
In skeletal muscle, contraction in a single fiber is all-ornone
In cardiac muscle, contraction can be graded: the fiber
can vary the amount of force it generates
The force generated is proportional to the number of
active crossbridges
Number of active crossbridges is determined by how
much Ca++ is bound to the troponin
Sarcomere length and contraction force
For both cardiac and skeletal muscle, the tension
generated by contraction is directly proportional to the
initial length of the muscle fiber
The longer the muscle fiber (and sarcomere) when a
contraction begins, the greater the tension developed,
up to a maximum
See next slide (fig. 14-12, p. 483)
Figure 14-12
Copyright © 2010 Pearson Education, Inc.
Action Potentials in Cardiac Muscle
Myocardial contractile cells (fig. 14-13)
Myocardial autorhythmic cells (fig. 14-15)
Action Potentials in Myocardial contractile cells
Action potential in these cells is very similar to the AP
in neurons and in skeletal muscle
Main difference: in Myocardium contractile cells, the
AP is a lot longer due to Ca++ entry
5 phases: 0, 1, 2, 3, 4
Figure 8-9, part 1
Action Potential in a Neuron
Fig. 8-9, p. 262
Copyright © 2010 Pearson Education, Inc.
Figure 14-13
Action Potential in a
cardiac contractile
cell
Copyright © 2010 Pearson Education, Inc.
Action Potentials in Myocardial contractile cells
Phase 4:
Resting Membrane Potential (RMP) of -90mV
Phase 0: Depolarization
Wave of depolarization moves into the fiber through
gap junctions
Voltage-gated Na+ channels open
Na+ enters cell, depolarizes it
Action Potentials in Myocardial contractile cells
Phase 1: Initial Repolarization
Very brief period
At +20mV, Na+ channels close
“Fast” K+ channels open
Cell begins to repolarize as K+ leaves
Phase 2: the Plateau
After the very brief phase 1, the AP flattens into a
plateau
2 events cause this
– A decrease in K+ permeability
• Some “fast” K+ channels close, K+ leaves
– An increase in Ca++ permeability
• Voltage-gated Ca++ channels began to slowly
open during phases 0 and 1
• At Phase 2, they are fully open and Ca++ enters
Phase 3: Rapid Repolarization
The plateau ends when Ca++ channels close and
“slow” K+ channels open
The “slow” K+ channels began to open during
depolarization (phase 0)
When they are finally completely open, K+ exits rapidly
and the cell returns to its RMP of -90mV
Figure 14-13
Copyright © 2010 Pearson Education, Inc.
1-5 msec:
Typical AP duration (neuron or skeletal muscle)
200+ msec:
Typical AP duration in a contractile myocardial cell
The influx of Ca++ during phase 2 lengthens the total
duration of the myocardial AP
The longer myocardial AP helps to prevent sustained
contraction (tetanus)
Prevention of tetanus in the heart muscle is important
because cardiac muscles have to relax between
contractions
During the relaxation phase, the ventricles fill with
blood
How does a longer AP prevent tetanus in the heart
muscle? (fig. 14-14, p. 485)
In skeletal muscle
– The AP (red curve) and refractory period (yellow
background) are ending as the contraction (blue
curve) begins
– A second AP, fired immediately after the refractory
period, causes summation of the contractions
– If a series of AP occur rapidly, then tetanus results
Figure 14-14
Copyright © 2010 Pearson Education, Inc.
How does a longer AP prevent tetanus in the heart
muscle? (fig. 14-14, p. 485)
In cardiac muscle
– The extended AP means that the refractory period
and the contraction end almost simultaneously
– By the time a second AP can occur, the
myocardial cell has almost completely relaxed
– Therefore, summation can't occur
Figure 14-14
Copyright © 2010 Pearson Education, Inc.
Table 14-3
Copyright © 2010 Pearson Education, Inc.
Myocardial Autorhythmic Cells (fig. 14-15)
These cells can spontaneously generate action
potentials without outside input
They can do this because they have an unstable
membrane potential, called a Pacemaker Potential
It is NOT a resting potential because it never “rests”
(never has a constant value)
Pacemaker potential starts at -60mV and slowly drifts
upward towards threshold
When it reaches threshold, it fires an AP
Figure 14-15a
Copyright © 2010 Pearson Education, Inc.
What Causes the Membrane Potential Instability?
Not fully understood yet
Current Hypothesis:
Autorhythmic cells contain a different kind of ion
channel called an If channel
The f subscript stands for “Funny”
These channels do not behave like other known
channels and were initially given the I f name
(I stands for current, so these were the “funny current”
channels)
What Causes the Membrane Potential Instability?
The If channels belong to the family of HCN channels
(hyperpolarization-activated cyclic nucleotide-gated
channels)
Other members of the HCN family are found in
neurons
What Causes the Membrane Potential Instability?
When the cell membrane potential is -60mV, then the I f
channels open
They are permeable to both K+ and Na+
When If channels open at negative membrane
potentials, Na+ influx exceeds K+ efflux
The net influx of positive charge slowly depolarizes the
autorhythmic cell
Figure 14-15
Copyright © 2010 Pearson Education, Inc.
What Causes the Membrane Potential Instability?
As the membrane potential becomes more positive,
the If channels gradually close and some Ca ++
channels open
Ca++ comes in and continues the depolarization
This moves the membrane potential steadily upwards
towards threshold
Figure 14-15
Copyright © 2010 Pearson Education, Inc.
What Causes the Membrane Potential Instability?
When the membrane potential reaches threshold,
additional Ca++ channels open
Ca++ rushes in, creating the steep depolarization
phase of the AP
Note: In other excitable cells, this phase is caused by
the opening of voltage-gated Na+ channels
Figure 14-15
Copyright © 2010 Pearson Education, Inc.
What Causes the Membrane Potential Instability?
When the Ca++ channels close (at the peak of the
AP), slow K+ channels are opening
The repolarization phase is due to the efflux of K+
Note: this phase is similar to repolarization in other
types of excitable cells
Figure 14-15
Copyright © 2010 Pearson Education, Inc.
Autonomic Neurotransmitters and Heart Rate
The speed at which pacemaker cells depolarize
determines the rate at which the heart contracts (heart
rate)
The interval between APs can be modified by altering
the permeability of the autorhythmic cells to different
ions
Autonomic Neurotransmitters and Heart Rate
Increased permeability to Na+ and Ca++ during the
pacemaker potential phase speeds up depolarization
and also heart rate
Decreased Ca++ permeability or increased K+
permeability slows down depolarization and also slows
down the heart rate
Autonomic Neurotransmitters and Heart Rate
Sympathetic stimulation of pacemaker cells speeds up
heart rate
The catecholamines Norepinephrine and Epinephrine
increase ion flow through both the I f and Ca++ channels
More rapid cation entry speeds up the rate of
pacemaker depolarization
This causes the cells to reach threshold faster and
increases the rate of AP firing, causing heart rate to
increase
Figure 14-16
Copyright © 2010 Pearson Education, Inc.
Autonomic Neurotransmitters and Heart Rate
Acetylcholine (Parasympathetic neurotransmitter)
slows down the heart rate
Acetylcholine activates muscarinic cholinergic
receptors that influence K+ and Ca++ channels in the
pacemaker cells
K+ permeability increases, hyperpolarizing the cell so
that the pacemaker potential begins at a more
negative value
Figure 14-16
Copyright © 2010 Pearson Education, Inc.
Autonomic Neurotransmitters and Heart Rate
At the same time, Ca++ permeability of the pacemaker
decreases
This slows the rate at which the pacemaker potential
depolarizes
The combination of the two effects causes the cell to
take longer to reach threshold, delaying the onset of
the AP in the pacemaker and slowing the heart rate
Figure 14-16
Copyright © 2010 Pearson Education, Inc.
The Heart as a Pump
Individual myocardial cells must depolarize and
contract in a coordinated fashion if the heart is to
create enough force to pump the blood throughout the
body
The signal sent out by the pacemaker coordinates the
actions of the individual myocardial cells
The Heart as a Pump
The pacemaker signal is electrical and spreads
throughout the heart muscle via gap junctions in the
intercalated disks
The depolarization wave is followed by a wave of
contraction
The wave passes first across the atria and then moves
down into the ventricles
Figure 14-17
Copyright © 2010 Pearson Education, Inc.
Depolarization begins in the Sinoatrial Node (SA)
pacemaker cells
located in the R. atrium and is the main pacemaker for
the heart
The depolarization wave spreads rapidly down to the
Atrioventricular node (AV node) through a branched
internodal pathway
Figure 14-18, overview
Copyright © 2010 Pearson Education, Inc.
Next, the depolarization wave travels from the AV
node down into the ventricles along the AV Bundle
Atrioventricular Bundle (AV Bundle or Bundle of His)
– Has Purkinje fibers
– These rapidly conduct the electrical signal down
the AV Bundle (up to 4 m/sec)
R. and L. Bundle Branches
– A short distance down the ventricular septum, the
AV Bundle splits into R. and L. branches
– These continue downward to the apex where they
divide into smaller fibers and spread out across
the ventricles
1. SA Node
2. AV Node
3. Bundle of His
4. R. and L.
Bundle
Branches
Figure 14-18, overview
Copyright © 2010 Pearson Education, Inc.
Heart Fibrous “Skeleton”
As the electrical signal spreads across the atria, it
encounters the fibrous skeleton (located between the
atria and ventricles)
This acts as an insulator
Prevents the electrical signal transferring from atria to
ventricles
Because of this insulation, the only pathway available
is from the AV node to the AV bundle, etc.
Atrioventricular (AV) Node
Why send electrical signals though the AV node?
Why not just let the signal spread downward from the
atria into the ventricles?
Atrioventricular (AV) Node
Answer:
Since blood is pumped out of the ventricles through
openings at the top of each chamber,
if the signal came directly down to the ventricles from
the atria, then the ventricles would start contracting
from the top
This would cause blood to be squeezed downward
and become trapped at the bottom of the ventricles
The apex to base contraction squeezes blood upwards
towards the arterial openings at the tops of the
ventricles
Ejection of blood
from the ventricles
is also helped by
the spiral arrangement
of the heart muscle
in the ventricle walls
Atrioventricular (AV) Node
The AV Node slightly delays transmission of the APs
in order to allow the atria to complete their contraction
before the ventricular contraction begins
This AV Node Delay works by slowing conduction
down through the nodal cells
Within the AV node, an action potential moves at only
1/20 the rate of an action potential in the atrial
inernodal pathway
Pacemakers
The fastest autorhythmic cells set the heart rate
Under normal conditions, the cells of the SA node are
the fastest (70 beats/minute)
If the SA node becomes damaged and can no longer
function properly, one of the other heart pacemakers
(autorhythmic cells) takes over
AV node: 50 beats/min
Purkinje fibers 25-40 beats/min
Fibrillation
Coordination of myocardial contraction is essential for
normal cardiac function
In extreme cases, when the cells contract in a
disorganized manner, fibrillation results
Atrial fibrillation
Fairly common, may not have symptoms, can become
quite serious (lead to strokes, etc.)
Ventricular fibrillation
Life threatening, emergency situation
Complete Heart Block
Conduction of electrical signals from the atria to the
ventricles through the AV node is disrupted
Sinoatrial Node still fires (at 70 beats/min), but the
signal never reaches the ventricles
The ventricles then coordinate with their fastest
pacemaker cells (at 35 beats/min)
Result: heart rate slows to 35 beats per/min, too slow
to maintain adequate blood flow
Treatment: artificial pacemaker
Go to Heart Part 3
Next: EKG on page 491