Download The Heart Part Two

THE CARDIOVASCULAR SYSTEM
Heart 2
PROPERTIES OF CARDIAC MUSCLE
Cardiac muscle
 Striated
 Short
 Wide
 Branched
 Interconnected
Skeletal muscle
 Striated
 Long
 Narrow
 Cylindrical
PROPERTIES OF CARDIAC MUSCLE
 Intercalated discs  passage of ions
 Numerous large mitochondria
 25–35% of cell volume
 Able to utilize many food molecules
 Example: lactic acid
Nucleus
Intercalated discs
Gap junctions
Cardiac muscle cell
Desmosomes
(a)
Figure 18.11a
Cardiac
muscle cell
Mitochondrion
Intercalated
disc
Nucleus
T tubule
Mitochondrion
Sarcoplasmic
reticulum
Z disc
Nucleus
Sarcolemma
(b)
I band
A band
I band
Figure 18.11b
PROPERTIES OF CARDIAC MUSCLE
 Some cells are myogenic
 Heart contracts as a unit or not at all
 Sodium channels leak slowly in specialized cells
 Spontaneous deoplarization
 Compare to skeletal muscle
Action Potential in Myogenic Cells of the Heart
Threshold
Action
potential
2
2
3
1
1
Pacemaker
potential
1 Pacemaker potential
2 Depolarization The
3 Repolarization is due to
This slow depolarization is
due to both opening of Na+
channels and closing of K+
channels. Notice that the
membrane potential is
never a flat line.
action potential begins when
the pacemaker potential
reaches threshold.
Depolarization is due to Ca2+
influx through Ca2+ channels.
Ca2+ channels inactivating and
K+ channels opening. This
allows K+ efflux, which brings
the membrane potential back
to its most negative voltage.
Figure 18.13
Action Potential of Contractile Cardiac Muscle Cells
1 Depolarization is
2
Tension
development
(contraction)
3
1
Absolute
refractory
period
Time (ms)
Tension (g)
Membrane potential (mV)
Action
potential
Plateau
due to Na+ influx through
fast voltage-gated Na+
channels. A positive
feedback cycle rapidly
opens many Na+
channels, reversing the
membrane potential.
Channel inactivation ends
this phase.
2 Plateau phase is
due to Ca2+ influx through
slow Ca2+ channels. This
keeps the cell depolarized
because few K+ channels
are open.
3 Repolarization is
due to Ca2+ channels
inactivating and K+
channels opening. This
allows K+ efflux, which
brings the membrane
potential back to its
resting voltage.
Figure 18.12
CONDUCTION SYSTEM OF THE HEART
 Terms
 Systole versus diastole
 Specialized cardiac cells
 Initiate impulse
 Conduct impulse
CONDUCTION SYSTEM OF THE HEART
 Conduction pathway
SA node (pacemaker)
AV node
purkinje fibers
atrial depolarization and contraction
bundle of His
myocardium
right and left bundle branches
contraction of ventricles
Conduction
Superior vena cava
Right atrium
Pathway
1 The sinoatrial (SA)
node (pacemaker)
generates impulses.
Internodal pathway
2 The impulses
pause (0.1 s) at the
atrioventricular
(AV) node.
3 The atrioventricular
(AV) bundle
connects the atria
to the ventricles.
4 The bundle branches
conduct the impulses
through the
interventricular septum.
5 The Purkinje fibers
Left atrium
Purkinje
fibers
Interventricular
septum
depolarize the contractile
cells of both ventricles.
(a) Anatomy of the intrinsic conduction system showing the
sequence of electrical excitation
(Intrinsic Innervation)
Figure 18.14a
CONDUCTION SYSTEM OF THE HEART
1.
Sinoatrial (SA) node (pacemaker)


2.
Generates impulses about 70-75 times/minute (sinus rhythm)
Depolarizes faster than any other part of the myocardium
Atrioventricular (AV) node


Delays impulses approximately 0.1 second
Depolarizes 50 times per minute in absence of SA node input
CONDUCTION SYSTEM OF THE HEART
3.
Atrioventricular (AV) bundle (bundle of His)

4.
Only electrical connection between the atria and ventricles
Right and left bundle branches

5.
Two pathways in the interventricular septum that carry the
impulses toward the apex of the heart
Purkinje fibers

Complete the pathway into the apex and ventricular walls
CONDUCTION SYSTEM OF THE HEART
 Intrinsic innervation
 External influences
 Normal :
 Average = 70 bpm
 Range = 60-100 bpm
The vagus nerve
(parasympathetic)
decreases heart rate.
Dorsal motor nucleus of vagus
Cardioinhibitory center
Medulla oblongata
Cardioacceleratory
center
Sympathetic trunk ganglion
Thoracic spinal cord
Sympathetic trunk
Sympathetic cardiac
nerves increase heart rate
and force of contraction.
AV node
SA node
Parasympathetic fibers
Sympathetic fibers
Interneurons
Figure 18.15
HOMEOSTATIC IMBALANCES
Defects in the intrinsic conduction system may result in
1.
2.
3.
4.
Arrhythmias: irregular heart rhythms
Bradycardia < 60 bpm
Tachycardia >100 bpm
Maximum is about 300 bpm
ELECTROCARDIOGRAPHY
 A composite of all the action potentials generated
by nodal and contractile cells at a given time
 Represents movement of ions = bioelectricity
 Three waves
1.
2.
3.
P wave: electrical depolarization of atria
QRS complex: ventricular depolarization
T wave: ventricular repolarization
QRS complex
Sinoatrial
node
Atrial
depolarization
Ventricular
depolarization
Ventricular
repolarization
Atrioventricular
node
P-Q
Interval
S-T
Segment
Q-T
Interval
Figure 18.16
SA node
Depolarization
R
Repolarization
R
T
P
S
1 Atrial depolarization, initiated
by the SA node, causes the
P wave.
R
AV node
T
P
Q
Q
S
4 Ventricular depolarization
is complete.
R
T
P
T
P
Q
S
2 With atrial depolarization
complete, the impulse is
delayed at the AV node.
R
Q
S
5 Ventricular repolarization
begins at apex, causing the
T wave.
R
T
P
T
P
Q
S
3 Ventricular depolarization
begins at apex, causing the
QRS complex. Atrial
repolarization occurs.
Q
S
6 Ventricular repolarization
is complete.
Figure 18.17
(a) Normal sinus rhythm.
(b) Junctional rhythm. The SA
node is nonfunctional, P waves
are absent, and heart is paced by
the AV node at 40 - 60 beats/min.
(c) Second-degree heart block. (d) Ventricular fibrillation. These
chaotic, grossly irregular ECG
Some P waves are not conducted
deflections are seen in acute
through the AV node; hence more
heart attack and electrical shock.
P than QRS waves are seen. In
this tracing, the ratio of P waves
to QRS waves is mostly 2:1.
Figure 18.18
THE CARDIAC CYCLE
 All events associated with blood flow through the
heart during one complete heartbeat
 Systole—contraction (ejection of blood)
 Diastole—relaxation (receiving of blood)
THE CARDIAC CYCLE
 Three events
1) Recordable bioelectrical disturbances (EKG)
2) Contraction of cardiac muscle
3) Generation of pressure and volume changes
 Blood flows from areas of higher pressure to areas of
lower pressure
 Valves prevent backflow
THE CARDIAC CYCLE
 Ventricular filling
ventricular systole
 Backpressure closes AV valves = isovolumetric contraction
 Ventricular pressure > aortic pressure
semilunar valves open
 Portion of ventricular contents ejected
Left heart
QRS
P
Electrocardiogram
EKG
T
1st
Heart sounds
P
2nd
Pressure (mm Hg)
Dicrotic notch
Aorta
Left ventricle
Atrial systole
Ventricular
volume (ml)
Pressure
changes
Changes in
volume
Left atrium
EDV
SV
ESV
Atrioventricular valves
Aortic and pulmonary valves
Phase
Contraction
Open
Closed
Open
Closed
Open
Closed
1
2a
2b
3
1
Left atrium
Right atrium
Left ventricle
Right ventricle
Ventricular
filling
Atrial
contraction
1
Ventricular filling
(mid-to-late diastole)
Isovolumetric
contraction phase
2a
Ventricular
ejection phase
2b
Ventricular systole
(atria in diastole)
Isovolumetric
relaxation
3
Ventricular
filling
Early diastole
Figure 18.20
HEART SOUNDS
 Two sounds associated with closing of heart valves
 First sound occurs as AV valves close and signifies beginning of
systole = Lub
 Second sound occurs when SL valves close at the beginning of
ventricular diastole = Dub
 Heart murmurs = abnormal heart sounds
 Most often indicative of valve problems
Aortic valve sounds heard
in 2nd intercostal space at
right sternal margin
Pulmonary valve
sounds heard in 2nd
intercostal space at left
sternal margin
Mitral valve sounds
heard over heart apex
(in 5th intercostal space)
in line with middle of
clavicle
Tricuspid valve sounds typically
heard in right sternal margin of
5th intercostal space
Figure 18.19
Left heart
QRS
Heart sounds
P
Electrocardiogram
T
1st
P
2nd
Pressure (mm Hg)
Dicrotic notch
Aorta
Left ventricle
Atrial systole
Ventricular
volume (ml)
Pressure
changes
Changes in
volume
Left atrium
EDV
SV
ESV
Atrioventricular valves
Aortic and pulmonary valves
Phase
Open
Closed
Open
Closed
Open
Closed
1
2a
2b
3
1
Left atrium
Right atrium
Left ventricle
Right ventricle
Ventricular
filling
Atrial
contraction
1
Ventricular filling
(mid-to-late diastole)
Isovolumetric
contraction phase
2a
Ventricular
ejection phase
2b
Ventricular systole
(atria in diastole)
Isovolumetric
relaxation
3
Ventricular
filling
Early diastole
Figure 18.20
HEART SOUNDS
 Mitral Stenosis
HEART SOUNDS
 Valvular insufficiency (regurgitation)
CARDIAC OUTPUT (CO)
 Definition: volume of blood pumped by each ventricle
in one minute
 Minute volume
 2 major factors
 Stroke volume
 Heart rate
CARDIAC OUTPUT
 CO (ml/min) = heart rate (HR) x stroke volume (SV)
 HR = number of beats per minute
 SV = volume of blood pumped out by a ventricle with each beat
(ml/min)
CARDIAC OUTPUT
 Stroke volume
 Difference between EDV and ESV
 EDV-ESV=SV
 Average is about 75 ml
Left heart
QRS
P
Electrocardiogram
EKG
T
1st
Heart sounds
P
2nd
Pressure (mm Hg)
Dicrotic notch
Aorta
Left ventricle
Atrial systole
Ventricular
volume (ml)
Pressure
changes
Changes in
volume
Left atrium
EDV
SV
ESV
Atrioventricular valves
Aortic and pulmonary valves
Phase
Open
Closed
Open
Closed
Open
Closed
1
2a
2b
3
1
Left atrium
Right atrium
Left ventricle
Right ventricle
Ventricular
filling
Atrial
contraction
1
Ventricular filling
(mid-to-late diastole)
Isovolumetric
contraction phase
2a
Ventricular
ejection phase
2b
Ventricular systole
(atria in diastole)
Isovolumetric
relaxation
3
Ventricular
filling
Early diastole
Figure 18.20
CARDIAC OUTPUT (CO)
 At rest
 CO (ml/min) = HR (75 beats/min)  SV (70 ml/beat)
= 5.25 L/min
 Maximal CO is 4–5 times resting CO in nonathletic people
 CO may reach 30 L/min in trained athletes
 Cardiac reserve
 Difference between resting and maximal CO
THOUGHT QUESTION
 If you increase stroke volume what would happen to
cardiac output?
Remember: CO = HR x SV
REGULATION OF STROKE VOLUME
 Stroke Volume
 Three main factors affect SV
 Preload
 Contractility
 Afterload
REGULATION OF STROKE VOLUME
 Preload
 Frank-Starling law of the heart
 Degree of stretch of cardiac muscle cells before they
contract
 Cardiac muscle exhibits a length-tension relationship
 At rest, cardiac muscle cells are shorter than optimal
length
 Slow heartbeat and exercise increase venous return
 Increased venous return distends (stretches) the
ventricles and increases contraction force
REGULATION OF STROKE VOLUME
 Contractility
 Contractile strength at a given muscle length,
independent of muscle stretch and EDV
 Agents increasing contractility
 Increased Ca2+ influx
 Sympathetic stimulation
 Hormones
 Thyroxin, glucagon, and epinephrine
 Agents decreasing contractility
 Calcium channel blockers
Increase SV
Decrease ESV
REGULATION OF STROKE VOLUME
 Afterload
 Pressure that must be overcome for ventricles to eject blood
 Hypertension increases afterload
 Results in increased ESV and reduced SV
CONTROL OF HEART RATE
 Sympathetic nervous system
 Norepinephrine
 Increased SA node firing rate
 Faster conduction through AV node
 Increases excitability of heart
 Parasympathetic nervous system
 Vagus nerve
 Decreases HR
Who dominates at rest?
Exercise (by
skeletal muscle and
respiratory pumps;
see Chapter 19)
Heart rate
(allows more
time for
ventricular
filling)
Bloodborne
epinephrine,
thyroxine,
excess Ca2+
Venous
return
Contractility
EDV
(preload)
ESV
Exercise,
fright, anxiety
Sympathetic
activity
Parasympathetic
activity
Heart
rate
Stroke
volume
Cardiac
output
Initial stimulus
Physiological response
Result
Figure 18.22
The vagus nerve
(parasympathetic)
decreases heart rate.
Dorsal motor nucleus of vagus
Cardioinhibitory center
Medulla oblongata
Cardioacceleratory
center
Sympathetic trunk ganglion
Thoracic spinal cord
Sympathetic trunk
Sympathetic cardiac
nerves increase heart rate
and force of contraction.
AV node
SA node
Parasympathetic fibers
Sympathetic fibers
Interneurons
Figure 18.15
CONTROL OF HEART RATE
 Other factors…
QUESTIONS?