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HEART
Part 2
A&P
Instructor Terry Wiseth
HEART CONDUCTION
Throughout the heart are clumps of
specialized cardiac muscle tissue whose
fibers contain only a few myofibrils
Initiate and distribute cardiac impulses
throughout the myocardium
2
HEART CONDUCTION
intrinsic ability to
generate and
conduct nerve
impulses
conducts impulse for
proper contraction
sequence of heart
3
HEART CONDUCTION
intrinsic ability to generate and conduct
nerve impulses
conducts impulse for proper contraction
sequence of heart
4
HEART CONDUCTION
intrinsic ability to generate and conduct
nerve impulses
conducts impulse for proper contraction
sequence of heart
5
SINOATRIAL NODE
Cell area located on the posterior part of
the right atrial wall, adjacent to the
junction of the superior vena cava and the
right atrium
“Pacemaker”
signals atria to contract
6
SINOATRIAL NODE
depolarization of the SA node is the first
step of the cardiac cycle
does not produce enough energy to be
recorded by the EEG
cells in the SA node
transmit impulses six
times faster than do
ordinary cell-to-cell
interconnections
7
SINOATRIAL NODE
The SA node sets the heart rate at 95
beats per minute
60 beats per minute is intrinsic to the
atria alone
20 - 40 beats per minute
is intrinsic to the
ventricles alone
8
HEART CONDUCTION
SINOATRIAL NODE
Acetycholine released by parasympathetic
system of ANS slows SA node to 72 beats
per minute
Other hormones affect heart rate by
influencing SA node
10
ECTOPIC PACEMAKER
Site other than SA node
develops an abnormal
self-excitability
Produces extra beats
Irregularly pace the
heart for short periods
of time
Nicotine and caffeine
can trigger these events
11
ATRIOVENTRICULAR NODE
made up of another cluster of specialized
cardiac conduction system cells
forms a pathway for impulse conduction
that bridges between the atria and
ventricles
delays impulse for atria to
finish contraction
12
HEART CONDUCTION
ATRIOVENTRICULAR NODE
Depolarization of the AV node is relatively
slow due to the intrinsic characteristics of
its cells
This causes a delay in the transmission of
the depolarization wave to the ventricles
transmission of the wave through the AV
node is relatively weak
considered silent on the
electrocardiogram
14
ATRIOVENTRICULAR NODE
damaged AV node
ventricles contract intrinsically slower
may require an artificial pacemaker
15
BUNDLE OF HIS
a compact tract of cardiac conduction
system fibers
also called the AV bundle
route for signals to leave the AV node
16
BUNDLE OF HIS
tract down the interventricular septum
The right and left branches spread the
electrical impulse to the right and left
ventricles
17
PURKINJE FIBERS
conduction system fibers which form a
rapid conduction network within the
myocardium
located at the ends of the bundle branches
18
PURKINJE FIBERS
responsible for propagating the
depolarization wave to all cardiac muscle
cells
The QRS Complex of the
electrocardiogram represents the
ventricular depolarization of contraction
19
HEART CONDUCTION
CONDUCTION
SA node
AV node
bundle of His
Purkinje fibers
CONDUCTION
Contraction begins at the heart apex and
progresses upwards
milking action of ventricular contraction
and the spiral arrangement of the
ventricular muscle fibers twist and wring
out the blood
22
HEART CONDUCTION
CONTROL OF CONTRACTION
brain is able to affect heart rate via
1) parasympathetic nerve impulses
heart-slowing
2) sympathetic nerve impulses
increase heart rate
24
CONTROL OF CONTRACTION
Click to View
Baroreceptor
control of
heart rate
CARDIAC RHYTHM
normal resting
70-80 beats/min
Systole
Contraction
Diastole
Expansion
26
VENTRICULAR DIASTOLE
during ventricular diastole cusps hang
loosely into ventricular chamber
27
VENTRICULAR SYSTOLE
during (at start of ) ventricular systole the
resulting increased blood pressure
developing in the ventricle forces the
flaps up together shutting the AV valves
28
VENTRICULAR SYSTOLE
semilunar valves forced open
29
VENTRICULAR DIASTOLE
semilunar valves
closed from back
flow pressure of
aortic and
pulmonary trunks
30
HEART SOUNDS
Lubb - dupp sounds are due to vibrations
in the heart tissues
created as the blood flow is suddenly
increased or slowed with the
contraction and relaxation of the heart
chambers
created with the opening and closing of
the valves
31
HEART SOUNDS
closing of valves causes vibrations in
heart wall
“lubb-dupp” sound of heartbeat
“lubb” S1
lower, louder
closing of AV valves
start of ventricular systole
“dupp” S2
softer, sharper
closing of semilunar valves
end of ventricular systole
32
ELECTROCARDIGRAM
Comprehensive image of the hearts
electrical activity
supplies a composite recording of all
action potentials produced by nodal and
muscle cells
three principle deflections
P wave
QRS complex
T wave
33
EKG COMPONENTS
EKG COMPONENTS
P WAVE
Signal from the SA node spreads through
the atria
atrial systole
36
QRS COMPLEX
Firing of SA node
ventricular systole
37
S-T SEGMENT
Following ventricular contraction and the
QRS complex is a brief period of low
electrical activity
On the electrocardiogram this appears
as the S-T segment
38
T WAVE
Ventricular repolarization is represented
by the T-wave on the electrocardiogram
The T-wave deflection is also in the same
direction of the largest deflection of the
QRS complex
39
EKG SUMMARY
depolarization
repolarization
READING EKG
Important to note the size of the deflection
waves at certain time intervals
41
ENLARGEMENT OF P-WAVE
Indicates
enlargement of the atria
atrial stenosis
mitral valve narrows
blood backs into the left atrium and
there is an expansion of the atrial wall
42
LENGTHENED P-R INTERVAL
Occurs because the heart tissue, covered
by the P-Q interval, namely the atria and AV node is scarred or inflamed
Impulse, as a result, travels at a slower rate
and the interval is lengthened
Atherosclerotic disease
Rheumatic fever
43
ENLARGED Q-WAVES AND R-WAVES
Enlarged R wave generally indicates
enlarged ventricles
Enlarged Q-wave may indicate a
myocardial infarction
44
S-T SEGMENT
Elevated S-T segment
acute myocardial infarction
Depressed S-T segment
heart muscle receives insufficient
oxygen
45
T-WAVE
Flat when the heart muscle is receiving
insufficient oxygen
May be elevated during hyperkalemia
High levels of potassium in bloodstream
46
CARDIAC CYCLE
1) Ventricular filling
2) Atrial systole
3) Isovolumetric ventricular contraction
4) Rapid ventricular ejection
5) Isovolumetric ventricular relaxation
47
1) VENTRICULAR FILLING
AV valves open due to low ventricular
pressure
blood passively enters the ventricles
P wave starts
48
2) ATRIAL SYSTOLE
SA node fires
contraction of the atrium stops the
pulmonary venous and systemic inflow
atrial contraction completes the filling of
the ventricles
pressure in the ventricles
increases closing the
AV valves
phase is indicated by the
P wave
49
3) ISOVOLUMETRIC CONTRACTION
ventricular contraction causes the
pressure to rise in the ventricles
AV valves close
blood is not ejected from the ventricles
atria relax
heart sound S1
phase is indicated
by the QRS complex
50
4) VENTRICULAR EJECTION
the pressure in the ventricles exceed the
pulmonary and systemic pressures
causing the semilunar valves to open
ventricle continues to contract rapidly
ejecting blood to the aorta
and pulmonary trunk
51
4) VENTRICULAR EJECTION
Ventricle contains 130 ml blood
EDV (End Diastolic Volume)
ventricles eject 54% (ejection fraction) of
the EDV during contraction
blood remaining behind is called ESV
(End Systolic Volume)
during rigorous exercise 90% may be
ejected
ejection fraction is an important measure
of cardiac health
52
5) ISOVOLUMETRIC RELAXATION
Ventricles expand causing pressure to
drop
semilunar valves close as the ventricular
pressure falls below the systemic and
pulmonary diastolic level
53
5) ISOVOLUMETRIC RELAXATION
ventricular pressures continue to fall until
it is slightly below atrial pressure
AV valves open
blood begins to fill the ventricles
phase is indicated
by the T wave
heart sound S2
54
CARDIAC CYCLE
VOLUME CHANGES
Ventricles pump as much blood as they
receive
both ventricles eject the same volume of
blood
ESV (leftover) 60 ml
atrial diastole +30 ml
atrial systole +40 ml
total EDV
130 ml
stroke volume -70 ml
ESV
60 ml
56
VOLUME CHANGES
If RV pumped more than LV could handle
on return
causes hypertension and edema in the
lungs
fluid swells the lungs
impairing gas
exchange
57
VOLUME CHANGES
If LV pumped more blood than RV can
handle on return
results in hypertension and edema in
the body
can lead to aneurysms,
stroke, kidney failure,
heart failure
58
CONGESTIVE HEART FAILURE
Failure of either ventricle to eject blood
effectively
can be caused by:
1) myocardial infarcted weakened heart
muscle
2) chronic hypertension
3) valvular insufficiency
4) congenital defects
59
CONGESTIVE HEART FAILURE
Left ventricle failure
pulmonary edema
shortness of breath
sense of suffocation
Right ventricle failure
systemic edema
enlargement of liver
swelling of fingers, ankles, feet
60
CONGESTIVE HEART FAILURE
Left ventricle failure
pulmonary edema
shortness of breath
sense of suffocation
Right ventricle failure
systemic edema
enlargement of liver
swelling of fingers, ankles, feet
61
CARDIAC OUTPUT
volume pumped by each ventricle per
minute
 CO = Heart Rate (HR) X Stroke Volume (SV)
HR = 75 bpm
SV = 70 ml/beat
CO = 75 X 70 = 5,250 ml/min = 5.25 L/min
total volume of blood is 4-6 L
thus entire volume of body’s blood is
pumped through each minute
vigorous exercise increases CO up to 21
L/min
62
CARDIAC OUTPUT
Cardiac output and peripheral resistance
determine blood pressure
Healthy young adult
120 mm Hg/ 80 mm Hg
63
HEART RATE
Normal
72 bpm
Tachycardia
rate above 100 bpm
stress, anxiety, drugs, disease, elevated
body temperature
Bradycardia
HR below 60 bpm
sleep, well trained
athlete, low body temperature
64
STROKE VOLUME
Governed by three factors
1) pre-load
2) contractility
3) after-load
65
PRE-LOAD
Determined by volume of blood in
ventricles
stretched myocardial muscle is able to
contract more forcefully
thus expel more blood
and increasing CO
66
CONTRACTILITY
Refers to the strength of contraction for a
given pre-load
measures myocyte receptivity to
stimulation
solutions of glucagon and calcium
chloride are standard emergency
treatment for heart attacks
digitalis acts as a cardiac stimulant to
treat congestive heart failure
barbiturates are negative
agents which reduce myocyte
response to stimulation
67
AFTER-LOAD
Blood pressure in arteries outside the
semilunar valve
opposes the opening of semilunar valves
increased after-load reduces the stroke
volume
68
AFTER-LOAD
 arterial circulation impediments increase afterload
scar tissue (lung diseases)
emphysema, chronic bronchitis
 cor pulmonale
RV failure due to obstructed pulmonary
circulation
Emphysema
69
HEART ABORMALITIES
Cardiomyopathy
The myocardium
functions poorly and
the heart is large and
dilated
MYOCARDIAL INFARCTION
71
MYOCARDIAL INFARCTION
MI ,“heart attack”
Within the lumen of the
coronary can be seen a dark
red recent coronary
thrombosis
The dull red color to the
myocardium to the lower
right of the thrombus is
consistent with underlying
myocardial infarction
72
MYOCARDIAL INFARCTION
left ventricular wall
sectioned lengthwise to
reveal a recent
myocardial infarction
The center of the
infarct contains
necrotic muscle that
appears yellow-tan
Remaining viable
myocardium is reddishbrown
73
MYOCARDIAL INFARCTION
Myocardial infarction necrotic tissue
74
MYOCARDIAL INFARCTION
histological acute myocardial infarction
contraction band necrosis
myocardial fibers are beginning to lose
cross striations
nuclei are not
clearly visible
many irregular
darker pink wavy
contraction bands
extending across
the fibers
75
ATRIAL FLUTTER
Cells in the atria set off extra
contractions
the atria beats 400-500 beats per minute
early firing can cause premature
ventricular contractions (PVCs)
often due to irritation of the heart by
stimulants, emotional stress, or lack of
sleep
can lead to ventricular fibrillation
76
VENTRICULAR FIBRILLATION
An arrhythmia caused by electrical
signals arriving at different regions of the
myocardium at widely different times
squirming, uncoordinated contractions
“bag of worms”
no pumping of blood
ischemia rapidly follows
77
CARDIAC ARREST
A cessation of cardiac output
ventricles may be motionless or in
fibrillation
78
DEFIBRILLATION
Heart is given a strong electric shock with
a pair of electrodes
79
DEFIBRILLATION
Depolarizes the entire myocardium and
stops the fibrillation
hope that the SA node will resume in
sinus rhythm
Atrial fibrillation
Normal sinus rhythm
Defibrillation
shocks
80
PACEMAKER
A pacing system stimulates the heart
muscle with precisely timed discharges of
electricity
cause the heart to beat in a manner very
similar to a naturally occurring heart
rhythm
81
PACEMAKER
The pacemaker sends tiny
electrical impulses to start a heartbeat
The electrode is designed to relay
information (sense) about your heart's
own electrical activity to
the pacemaker and to
deliver electrical
impulses (paces) only
when the heart needs
them
82
PACEMAKER
DYNAMIC CARDIOMYOPLASTY
involves harvesting the the Latissimus
Dorsi
the muscle is wrapped around the surface
of the heart
the nerve to the muscle is stimulated
(with a specialized pacemaker device)
allowing the muscle to contract
improves the ejection of blood from the
heart
lessens the symptoms of heart failure
84
DYNAMIC CARDIOMYOPLASTY
DYNAMIC CARDIOMYOPLASTY
HYPERTENSION
The left ventricle is markedly thickened in
this patient with severe hypertension that
was untreated for many years
hypertension creates a greater pressure
load on the heart to induce the
hypertrophy
87
AORTIC TEAR
a sudden deceleration injury in a
vehicular accident can produce a tear in
the aorta
tear is just distal to the great vessels
the tear leads to sudden loss of blood and
shock
It is widely
believed that
Princess
Diana died
from an
aortic tear
brought on by
a sudden
deceleration
88
AORTIC TEAR
AORTIC TEAR
BACTERIAL INFECTION
Endocarditis
blue bacterial colonies on the lower left
extending into the pink connective
tissue of the valve
valves are relatively avascular
high dose antibiotic therapy is needed
to eradicate
the infection
91
BACTERIAL INFECTION
patient with infective endocarditis and
blood culture positive for Staphylococcus
aureus
small linear subungual splinter
hemorrhage
92
HEART TUMOR
heart of a two year old child who died
suddenly
at autopsy, a large firm, white tumor mass
was found filling much of the left ventricle
tumors of the
heart are rare
93
HEART TUMOR
PULMONARY
THROMBOEMBOLUS
Blood clots formed
elsewhere in the body
can dislodge and move
through the larger blood
vessels and heart and
become lodged in the
smaller pulmonary circuit
blood vessels causing a
blockage or bursting of
the blood vessel
HEART LUNG MACHINE
HEART LUNG MACHINE
FEET
BLUE
BLOOD TO
PUMP
RED
BLOOD TO
BODY
HEAD
ATRIAL SEPTAL DEFECT
A defect involving both the atrial and the
ventricular septums allows blood to pass
freely between the two ventricles and the
atriums
98
ATRIAL SEPTAL DEFECT
The valve apparatus at the junction
between atriums and ventricles is
"shared"
effectively only one valve instead of the
normal two
Blood flow and
pressure in the
lung circulation
is substantially
increased
99
ATRIAL SEPTAL DEFECT
often results in early onset of symptoms
with:
breathlessness
poor feeding
slow weight gain
defect is very
common in babies
with Down syndrome
100
VENTRICULAR SEPTAL DEFECT
FOSSA OVALIS
depression in interatrial septum
opening which exists in fetal heart
foramen ovale
RA
RV
102
HEART CHANGES AT BIRTH
At birth, the first breath inflates
the lungs
lowers the resistance to
blood flow
thus increases the volume of
blood flowing through them
thereby increasing the
amount of blood returning
from the pulmonary trunk to
the heart
all of which results in
increased pressure in the left
atrium
103
FETAL CIRCULATION
FETAL CIRCULATION
HEART CHANGES AT BIRTH
increased pressure in the left atrium
forces the flap covering the foramen
ovale against the interatrial septum
blocking off
communication
between the right
and left atrium
106
HEART CHANGES AT BIRTH
closure of the ductus arteriosus
takes place almost
immediately after birth
due to muscular contraction
mediated by, bradykinin
released from the lungs
after the newborn's first
breath
107
HEART CHANGES AT BIRTH
 In some instances, the ductus arteriosus
does not obliterate within the first few
days leaving a left to right shunt
108
HEART CHANGES AT BIRTH
There are two shortcuts; normally, both of
them close up at birth or shortly
thereafter
ductus arteriosus
a small blood vessel
connecting the
pulmonary artery
and aorta
foramen ovale
a small hole
between the left
and right atria
109
DUCTUS ARTERIOSUS
BEFORE AND AFTER
HEART CHANGES AT BIRTH
Openings and blood vessels close at birth
and if they do not two conditions may
result:
Patent Ductus Arteriosus (PDA)
Patent Foramen Ovale (PFO)
111
PATENT DUCTUS ARTERIOSUS
HEART CHANGES AT BIRTH
Either of these conditions can cause
fatigue
difficult or rapid breathing
failure to grow normally
chronic respiratory
infections
Large openings can lead
to heart failure and death
113
DUCTUS ARTERIOSUS REPAIR
END
HEART
Part 2