Download NURS1004 Week 10 Lecture the Heart Part II Prepared by Didy

NURS1004 Week 10 Lecture the
Heart Part II
Prepared by Didy Button.
20-2 The Conducting System
• Heartbeat
– A single contraction of the heart
– The entire heart contracts in series
• First the atria
• Then the ventricles
20-2 The Conducting System
• Cardiac Physiology
– Two Types of Cardiac Muscle Cells
1. Conducting system
–
Controls and coordinates heartbeat
2. Contractile cells
–
Produce contractions that propel blood
20-2 The Conducting System
• The Cardiac Cycle
– Begins with action potential at SA node
• Transmitted through conducting system
• Produces action potentials in cardiac muscle cells
(contractile cells)
– Electrocardiogram (ECG or EKG)
• Electrical events in the cardiac cycle can be recorded on
an electrocardiogram
20-2 The Conducting System
• The Conducting System
– A system of specialized cardiac muscle cells
• Initiates and distributes electrical impulses that
stimulate contraction
– Automaticity
• Cardiac muscle tissue contracts automatically
20-2 The Conducting System
• Structures of the Conducting System
– Sinoatrial (SA) node - wall of right atrium
– Atrioventricular (AV) node - junction between
atria and ventricles
– Conducting cells - throughout myocardium
20-2 The Conducting System
• Conducting Cells
– Interconnect SA and AV nodes
– Distribute stimulus through myocardium
– In the atrium
• Internodal pathways
– In the ventricles
• AV bundle and the bundle branches
20-2 The Conducting System
• Prepotential
– Also called pacemaker potential
– Resting potential of conducting cells
• Gradually depolarizes toward threshold
– SA node depolarizes first, establishing heart rate
ANIMATION The Heart: Conduction System
Figure 20-11a The Conducting System of the Heart
Sinoatrial
(SA) node
Internodal
pathways
Atrioventricular
(AV) node
AV bundle
Bundle
branches
Purkinje
fibers
Components of the conducting
system
Figure 20-11b The Conducting System of the Heart
Threshold
Prepotential
(spontaneous depolarization)
Time (sec)
Changes in the membrane potential of a pacemaker
cell in the SA node that is establishing a heart rate of
72 beats per minute. Note the presence of a
prepotential, a gradual spontaneous depolarization.
20-2 The Conducting System
• Heart Rate
– SA node generates 80–100 action potentials per
minute
– Parasympathetic stimulation slows heart rate
– AV node generates 40–60 action potentials per
minute
20-2 The Conducting System
• The Sinoatrial (SA) Node
– In posterior wall of right atrium
– Contains pacemaker cells
– Connected to AV node by internodal pathways
– Begins atrial activation (Step 1)
Figure 20-12 Impulse Conduction through the Heart (Step 1)
SA node activity
and atrial
activation begin.
Time = 0
SA
node
20-2 The Conducting System
• The Atrioventricular (AV) Node
– In floor of right atrium
– Receives impulse from SA node (Step 2)
– Delays impulse (Step 3)
– Atrial contraction begins
Figure 20-12 Impulse Conduction through the Heart (Step 2)
Stimulus spreads across
the atrial surfaces and
reaches the AV node.
AV
node
Elapsed time = 50 msec
Figure 20-12 Impulse Conduction through the Heart (Step 3)
There is a 100-msec delay
at the AV node. Atrial
contraction begins.
AV
bundle
Bundle
branches
Elapsed time = 150 msec
20-2 The Conducting System
• The AV Bundle
– In the septum
– Carries impulse to left and right bundle branches
• Which conduct to Purkinje fibers (Step 4)
– And to the moderator band
• Which conducts to papillary muscles
Figure 20-12 Impulse Conduction through the Heart (Step 4)
The impulse travels along
the interventricular septum
within the AV bundle and
the bundle branches to the
Purkinje fibers and, via the
moderator band, to the
papillary muscles of the
right ventricle.
Moderator
band
Elapsed time = 175 msec
20-2 The Conducting System
• Purkinje Fibers
– Distribute impulse through ventricles (Step 5)
– Atrial contraction is completed
– Ventricular contraction begins
Figure 20-12 Impulse Conduction through the Heart (Step 5)
The impulse is distributed
by Purkinje fibers and
relayed throughout the
ventricular myocardium.
Atrial contraction is
completed, and ventricular
contraction begins.
Purkinje
Elapsed time = 225 msec
fibers
20-2 The Conducting System
• Abnormal Pacemaker Function
– Bradycardia - abnormally slow heart rate
– Tachycardia - abnormally fast heart rate
– Ectopic pacemaker
• Abnormal cells
• Generate high rate of action potentials
• Bypass conducting system
• Disrupt ventricular contractions
20-2 The Conducting System
• The Electrocardiogram (ECG or EKG)
– A recording of electrical events in the heart
– Obtained by electrodes at specific body
locations
– Abnormal patterns diagnose damage
Figure 20-13a An Electrocardiogram
Electrode placement for
recording a standard ECG.
20-2 The Conducting System
• Features of an ECG
– P wave
• Atria depolarize
– QRS complex
• Ventricles depolarize
– T wave
• Ventricles repolarize
20-2 The Conducting System
• Time Intervals between ECG Waves
– P–R interval
• From start of atrial depolarization
• To start of QRS complex
– Q–T interval
• From ventricular depolarization
• To ventricular repolarization
Figure 20-13a An Electrocardiogram
Electrode placement for
recording a standard ECG.
Figure 20-13b An Electrocardiogram
800 msec
R
P wave
(atria
depolarize)
R
T wave
(ventricles repolarize)
P–R segment
S–T
segment
Millivolts
Q S
P–R
interval
S–T
interval
Q–T
interval
QRS interval
(ventricles depolarize)
Figure 20-14 Cardiac Arrhythmias
Premature Atrial Contractions (PACs)
P
P
P
Paroxysmal Atrial Tachycardia (PAT)
P
P
P
Atrial Fibrillation (AF)
P
P
P
Figure 20-14 Cardiac Arrhythmias
Premature Ventricular Contractions (PVCs)
P
T
P
T
Ventricular Tachycardia (VT)
P
Ventricular Fibrillation (VF)
P
T
20-2 The Conducting System
• Refractory Period
– Absolute refractory period
• Long
• Cardiac muscle cells cannot respond
– Relative refractory period
• Short
• Response depends on degree of stimulus
20-2 The Conducting System
• The Role of Calcium Ions in Cardiac
Contractions
– Contraction of a cardiac muscle cell
• Is produced by an increase in calcium ion
concentration around myofibrils
20-2 The Conducting System
• The Energy for Cardiac Contractions
– Aerobic energy of heart
• From mitochondrial breakdown of fatty acids and
glucose
• Oxygen from circulating hemoglobin
• Cardiac muscles store oxygen in myoglobin
20-3 The Cardiac Cycle
• The Cardiac Cycle
– Is the period between the start of one
heartbeat and the beginning of the next
– Includes both contraction and relaxation
20-3 The Cardiac Cycle
• Two Phases of the Cardiac Cycle
– Within any one chamber
1. Systole (contraction)
2. Diastole (relaxation)
Figure 20-16 Phases of the Cardiac Cycle
Start
0
800 msec
msec
100
msec
Cardiac
cycle
370
msec
Figure 20-16a Phases of the Cardiac Cycle
Start
Atrial systole begins:
Atrial contraction forces a small amount of
additional blood into relaxed ventricles.
0
800 msec
msec
Cardiac
cycle
100
msec
Figure 20-16b Phases of the Cardiac Cycle
Atrial systole ends,
atrial diastole
begins
100
msec
Cardiac
cycle
Figure 20-16c Phases of the Cardiac Cycle
Cardiac
cycle
Ventricular systole—
first phase: Ventricular
contraction pushes AV
valves closed but does
not create enough
pressure to open
semilunar valves.
Figure 20-16d Phases of the Cardiac Cycle
Cardiac
cycle
370
msec
Ventricular systole—
second phase: As
ventricular pressure rises
and exceeds pressure
in the arteries, the
semilunar valves
open and blood
is ejected.
Figure 20-16e Phases of the Cardiac Cycle
Cardiac
cycle
370
msec
Ventricular diastole—early:
As ventricles relax, pressure in
ventricles drops; blood flows back
against cusps of semilunar valves
and forces them closed. Blood
flows into the relaxed atria.
Figure 20-16f Phases of the Cardiac Cycle
800
msec
Cardiac
cycle
Ventricular
diastole—late:
All chambers are
relaxed.
Ventricles fill
passively.
20-3 The Cardiac Cycle
• Blood Pressure
– In any chamber
• Rises during systole
• Falls during diastole
– Blood flows from high to low pressure
• Controlled by timing of contractions
• Directed by one-way valves
20-3 The Cardiac Cycle
• Cardiac Cycle and Heart Rate
– At 75 beats per minute (bpm)
• Cardiac cycle lasts about 800 msec
– When heart rate increases
• All phases of cardiac cycle shorten, particularly diastole
20-3 The Cardiac Cycle
•
Phases of the Cardiac Cycle
– Atrial systole
– Atrial diastole
– Ventricular systole
– Ventricular diastole
20-3 The Cardiac Cycle
• Atrial Systole
1. Atrial systole
– Atrial contraction begins
– Right and left AV valves are open
2. Atria eject blood into ventricles
– Filling ventricles
3. Atrial systole ends
– AV valves close
– Ventricles contain maximum blood volume
– Known as end-diastolic volume (EDV)
20-3 The Cardiac Cycle
• Ventricular Systole
4. Ventricles contract and build pressure
• AV valves close cause isovolumetric contraction
5. Ventricular ejection
• Ventricular pressure exceeds vessel pressure opening the
semilunar valves and allowing blood to leave the ventricle
• Amount of blood ejected is called the stroke volume (SV)
20-3 The Cardiac Cycle
• Ventricular Systole
6. Ventricular pressure falls
• Semilunar valves close
• Ventricles contain end-systolic volume (ESV), about 40% of enddiastolic volume
Figure 20-17 Pressure and Volume Relationships in the Cardiac Cycle
ATRIAL
ATRIAL
DIASTOLE SYSTOLE
VENTRICULAR
DIASTOLE
ATRIAL DIASTOLE
VENTRICULAR
SYSTOLE
Aortic valve
opens
Aorta
Pressure
(mm Hg)
Atrial contraction begins.
Atria eject blood into ventricles.
Atrial systole ends; AV valves close.
Left
ventricle
Isovolumetric ventricular contraction.
Ventricular ejection occurs.
Semilunar valves close.
Isovolumetric relaxation occurs.
Left AV
valve closes
Left atrium
AV valves open; passive ventricular
filling occurs.
Left
ventricular
volume (mL)
End-diastolic
volume
Stroke
volume
Time (msec)
20-3 The Cardiac Cycle
• Ventricular Diastole
7. Ventricular diastole
• Ventricular pressure is higher than atrial pressure
• All heart valves are closed
• Ventricles relax (isovolumetric relaxation)
8. Atrial pressure is higher than ventricular pressure
• AV valves open
• Passive atrial filling
• Passive ventricular filling
Figure 20-17 Pressure and Volume Relationships in the Cardiac Cycle
ATRIAL
SYSTOLE
ATRIAL DIASTOLE
VENTRICULAR
SYSTOLE
VENTRICULAR DIASTOLE
Aortic valve
closes
Dicrotic
notch
Atrial contraction begins.
Pressure
(mm Hg)
Atria eject blood into ventricles.
Atrial systole ends; AV valves close.
Isovolumetric ventricular contraction.
Ventricular ejection occurs.
Semilunar valves close.
Left
ventricular
volume (mL)
Left AV
valve opens
End-systolic
volume
Time (msec)
Isovolumetric relaxation occurs.
AV valves open; passive ventricular
filling occurs.
20-3 The Cardiac Cycle
• Heart Sounds
– S1
• Loud sounds
• Produced by AV valves
– S2
• Loud sounds
• Produced by semilunar valves
ANIMATION The Heart: Cardiac Cycle
20-3 The Cardiac Cycle
• S3, S4
– Soft sounds
– Blood flow into ventricles and atrial contraction
• Heart Murmur
– Sounds produced by regurgitation through
valves
Figure 20-18a Heart Sounds
Sounds heard
Valve location
Aortic
valve
Valve location
Sounds heard
Pulmonary
valve
Sounds heard
Valve location
Left
AV
valve
Valve location
Sounds heard
Right
AV
valve
Placements of a stethoscope for
listening to the different sounds
produced by individual valves
Figure 20-18b Heart Sounds
Semilunar
valves close
Pressure
(mm Hg)
Semilunar
valves open
Left
ventricle
Left
atrium
AV valves
open
AV valves
close
S1
S4
S2
S3
Heart sounds
“Lubb”
“Dubb”
The relationship between heart sounds and key events in the
cardiac cycle
S4
20-4 Cardiodynamics
• Cardiodynamics
– The movement and force generated by cardiac
contractions
• End-diastolic volume (EDV)
• End-systolic volume (ESV)
• Stroke volume (SV)
– SV = EDV – ESV
• Ejection fraction
– The percentage of EDV represented by SV
Figure 20-19 A Simple Model of Stroke Volume
Start
Filling
Ventricular
diastole
End-systolic
volume
(ESV)
End-diastolic
volume (EDV)
Stroke
volume
Pumping
Ventricular
systole
Figure 20-19 A Simple Model of Stroke Volume
Start
When the pump handle is
raised, pressure within the
cylinder decreases, and
water enters through a
one-way valve. This
corresponds to passive
filling during ventricular
diastole.
Filling
Ventricular
diastole
Figure 20-19 A Simple Model of Stroke Volume
At the start of the pumping
cycle, the amount of water in
the cylinder corresponds to the
amount of blood in a ventricle
at the end of ventricular
diastole. This amount is known
as the end-diastolic volume
(EDV).
End-diastolic
volume (EDV)
Figure 20-19 A Simple Model of Stroke Volume
Pumping
Ventricular
systole
As the pump handle is
pushed down, water is forced
out of the cylinder. This corresponds to the period of
ventricular ejection.
Figure 20-19 A Simple Model of Stroke Volume
End-systolic
volume
(ESV)
Stroke
volume
When the handle is depressed as
far as it will go, some water will
remain in the cylinder. That amount
corresponds to the end-systolic
volume (ESV) remaining in the
ventricle at the end of ventricular
systole. The amount of water
pumped out corresponds to the
stroke volume of the heart; the
stroke volume is the difference
between the EDV and the ESV.
20-4 Cardiodynamics
• Cardiac Output (CO)
– The volume pumped by left ventricle in 1
minute
– CO = HR  SV
• CO = cardiac output (mL/min)
• HR = heart rate (beats/min)
• SV = stroke volume (mL/beat)
Figure 20-20 Factors Affecting Cardiac Output
Factors Affecting
Heart Rate (HR)
Autonomic
innervation
Hormones
HEART RATE (HR)
Factors Affecting
Stroke Volume (SV)
End-diastolic
volume
End-systolic
volume
STROKE VOLUME (SV) = EDV – ESV
CARDIAC OUTPUT (CO) = HR  SV
20-4 Cardiodynamics
• Autonomic Innervation
– Cardiac plexuses innervate heart
– Vagus nerves (N X) carry parasympathetic
preganglionic fibers to small ganglia in cardiac
plexus
– Cardiac centers of medulla oblongata
• Cardioacceleratory center controls sympathetic neurons
(increases heart rate)
• Cardioinhibitory center controls parasympathetic neurons (slows
heart rate)
20-4 Cardiodynamics
• Autonomic Innervation
– Cardiac reflexes
• Cardiac centers monitor:
– Blood pressure (baroreceptors)
– Arterial oxygen and carbon dioxide levels (chemoreceptors)
– Cardiac centers adjust cardiac activity
– Autonomic tone
• Dual innervation maintains resting tone by releasing ACh and NE
• Fine adjustments meet needs of other systems
Figure 20-21 Autonomic Innervation of the Heart
Vagal nucleus
Cardioinhibitory
center
Cardioacceleratory
center
Medulla
oblongata
Vagus (N X)
Spinal cord
Sympathetic
Sympathetic
ganglia (cervical
ganglia and
superior thoracic
ganglia [T1–T4])
Sympathetic
preganglionic
fiber
Sympathetic
postganglionic fiber
Cardiac nerve
Parasympathetic
Parasympathetic
preganglionic
fiber
Synapses in
cardiac plexus
Parasympathetic
postganglionic
fibers
20-4 Cardiodynamics
• Effects on the SA Node
– Membrane potential of pacemaker cells
• Lower than other cardiac cells
– Rate of spontaneous depolarization depends on:
• Resting membrane potential
• Rate of depolarization
Figure 20-22a Autonomic Regulation of Pacemaker Function
Normal (resting)
Prepotential
(spontaneous
depolarization)
Membrane
potential
(mV)
Threshold
Heart rate: 75 bpm
Pacemaker cells have membrane potentials closer to threshold
than those of other cardiac muscle cells (–60 mV versus
–90 mV). Their plasma membranes undergo spontaneous
depolarization to threshold, producing action potentials at a
frequency determined by (1) the resting-membrane potential
and (2) the rate of depolarization.
20-4 Cardiodynamics
• Effects on the SA Node
– Sympathetic and parasympathetic stimulation
• Greatest at SA node (heart rate)
– ACh (parasympathetic stimulation)
• Slows the heart
– NE (sympathetic stimulation)
• Speeds the heart
Figure 20-22b Autonomic Regulation of Pacemaker Function
Parasympathetic stimulation
Membrane
potential
(mV)
Threshold
Hyperpolarization
Heart rate: 40 bpm
Slower depolarization
Parasympathetic stimulation releases ACh, which
extends repolarization and decreases the rate of
spontaneous depolarization. The heart rate slows.
Figure 20-22c Autonomic Regulation of Pacemaker Function
Sympathetic stimulation
Membrane
potential
(mV)
Threshold
Reduced repolarization
Heart rate: 120 bpm
More rapid
depolarization
Time (sec)
Sympathetic stimulation releases NE, which shortens
repolarization and accelerates the rate of spontaneous
depolarization. As a result, the heart rate increases.
20-4 Cardiodynamics
• Atrial Reflex
– Also called Bainbridge reflex
– Adjusts heart rate in response to venous return
– Stretch receptors in right atrium
• Trigger increase in heart rate
• Through increased sympathetic activity
20-4 Cardiodynamics
• Hormonal Effects on Heart Rate
– Increase heart rate (by sympathetic stimulation
of SA node)
• Epinephrine (E)
• Norepinephrine (NE)
• Thyroid hormone
20-4 Cardiodynamics
• Factors Affecting the Stroke Volume
– The EDV amount of blood a ventricle contains at
the end of diastole
• Filling time
– Duration of ventricular diastole
• Venous return
– Rate of blood flow during ventricular diastole
20-4 Cardiodynamics
• Preload
– The degree of ventricular stretching during
ventricular diastole
– Directly proportional to EDV
– Affects ability of muscle cells to produce tension
20-4 Cardiodynamics
• The EDV and Stroke Volume
– At rest
• EDV is low
• Myocardium stretches less
• Stroke volume is low
– With exercise
• EDV increases
• Myocardium stretches more
• Stroke volume increases
20-4 Cardiodynamics
• The Frank–Starling Principle
– As EDV increases, stroke volume increases
• Physical Limits
– Ventricular expansion is limited by:
• Myocardial connective tissue
• The cardiac (fibrous) skeleton
• The pericardial sac
20-4 Cardiodynamics
• End-Systolic Volume (ESV)
– Is the amount of blood that remains in the
ventricle at the end of ventricular systole
20-4 Cardiodynamics
• Three Factors That Affect ESV
1. Preload
• Ventricular stretching during diastole
2. Contractility
• Force produced during contraction, at a given preload
3. Afterload
• Tension the ventricle produces to open the semilunar
valve and eject blood
20-4 Cardiodynamics
• Contractility
– Is affected by:
• Autonomic activity
• Hormones
20-4 Cardiodynamics
• Effects of Autonomic Activity on Contractility
– Sympathetic stimulation
• NE released by postganglionic fibers of cardiac nerves
• Epinephrine and NE released by adrenal medullae
• Causes ventricles to contract with more force
• Increases ejection fraction and decreases ESV
20-4 Cardiodynamics
• Effects of Autonomic Activity on
Contractility
– Parasympathetic activity
• Acetylcholine released by vagus nerves
• Reduces force of cardiac contractions
20-4 Cardiodynamics
• Afterload
– Is increased by any factor that restricts arterial
blood flow
– As afterload increases, stroke volume
decreases
Figure 20-23 Factors Affecting Stroke Volume
Factors Affecting Stroke Volume (SV)
Venous return (VR)
VR =
VR =
EDV
EDV
Filling time (FT)
FT = EDV
FT = EDV
Increased by
sympathetic
stimulation
Decreased by
parasympathetic
stimulation
Increased by E, NE,
glucagon,
thyroid hormones
Contractility (Cont)
of muscle cells
Cont =
Cont =
Preload
End-diastolic
volume (EDV)
ESV
ESV
End-systolic
volume (ESV)
STROKE VOLUME (SV)
EDV =
EDV =
SV
SV
ESV =
ESV =
SV
SV
Increased by
vasoconstriction
Decreased by
vasodilation
Afterload (AL)
AL = ESV
AL = ESV
20-4 Cardiodynamics
• Summary: The Control of Cardiac Output
– Heart Rate Control Factors
• Autonomic nervous system
– Sympathetic and parasympathetic
• Circulating hormones
• Venous return and stretch receptors
20-4 Cardiodynamics
• Summary: The Control of Cardiac Output
– Stroke Volume Control Factors
• EDV
– Filling time, and rate of venous return
• ESV
– Preload, contractility, afterload
20-4 Cardiodynamics
• Cardiac Reserve
– The difference between resting and maximal
cardiac output
20-4 Cardiodynamics
• The Heart and Cardiovascular System
– Cardiovascular regulation
• Ensures adequate circulation to body tissues
– Cardiovascular centers
• Control heart and peripheral blood vessels
– Cardiovascular system responds to:
• Changing activity patterns
• Circulatory emergencies
Figure 20-24 A Summary of the Factors Affecting Cardiac Output
Factors affecting heart fate (HR)
Factors affecting stroke volume (SV)
Skeletal Blood Changes in
muscle volume peripheral
activity
circulation
Venous
return
Atrial
reflex
Autonomic
innervation
Hormones
HEART RATE (HR)
Filling
time
Autonomic
innervation
Preload
Contractility
End-diastolic
volume
End-systolic
volume
Hormones
STROKE VOLUME (SV) = EDV – ESV
CARDIAC OUTPUT (CO) = HR  SV
Vasodilation or
vasoconstriction
Afterload