Transcript Cardiac Cycle - HCC Learning Web

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 end-
diastolic 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)
20-4 Cardiodynamics
• Factors Affecting Cardiac Output
– Cardiac output
• Adjusted by changes in heart rate or stroke volume
– Heart rate
• Adjusted by autonomic nervous system or hormones
– Stroke volume
• Adjusted by changing EDV or ESV
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)
Membrane
potential
(mV)
Prepotential
(spontaneous
depolarization)
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
More rapid
depolarization
Heart rate: 120 bpm
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
• Hormones
– Many hormones affect heart contraction
– Pharmaceutical drugs mimic hormone actions
• Stimulate or block beta receptors
• Affect calcium ions (e.g., calcium channel blockers)
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 = EDV
VR = 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
muscle
activity
Blood
volume
Venous
return
Atrial
reflex
Changes in
peripheral
circulation
Filling
time
Preload
Autonomic
innervation
End-diastolic
volume
Hormones
HEART RATE (HR)
Autonomic
innervation
Contractility
End-systolic
volume
STROKE VOLUME (SV) = EDV – ESV
CARDIAC OUTPUT (CO) = HR  SV
Hormones
Vasodilation or
vasoconstriction
Afterload