the heart

1
Chapter 20
the heart
2
Anatomy review Electrical activity of the whole
heart (EKG) Electrical activity of the heart
cells The Cardiac Cycle Cardiac Input and
Output (dynamics)
3
Heart review
4 chambers 2 atria 2 ventricles 4 valves 2 AV
valves 2 semilunar valves 2 circuits systemic
pulmonary
receive send
4
external heart anatomy
fig. 20-9
5
internal heart anatomy
fig. 20-6
6
100 keys (pg. 678)
The heart has four chambers, two associated with
the pulmonary circuit (right atrium and right
ventricle) and two with the systemic circuit
(left atria and left ventricle). The left
ventricle has a greater workload and is much more
massive than the right ventricle, but the two
chambers pump equal amounts of blood. AV valves
prevent backflow from the ventricles into the
atria, and semilunar valves prevent backflow from
the aortic and pulmonary trunks into the
ventricles.
7
cardiac conduction system
modified cardiac muscle cells

• SA node (sinoatrial node)
• wall of RA
• AV node (atrioventricular node)
• between atrium and ventricle
• conducting cells
• AV bundle (of His)
• conducting fibers
• Purkinje fibers

8
conducting system of heart
fig. 20-12a
9
prepotential
cannot maintain steady resting potential gradually
drift toward threshold
SA node 80-100 bpm AV node 40-60 bpm
10
fig. 20-12b
11
because SA node is faster
it controls the heart rate (pacemaker)
but heart rate is normally slower than 80-100
bpm (parasympathetics)
if SA node is damaged, heart can still continue
to beat, but at a slower rate
12
if heartbeat is slower than normal
bradycardia if heartbeat is faster than
normal tachycardia
13
impulse conduction
fig. 20-13
14
impulse conduction
SA node atria get signal - contract signal to
AV Node AV node sends signal to ventricles
(time delay) ventricles contract after
atria are done
damage to any part of conducting system may
result in abnormalities (EKG)
15
ECGs EKGs
electrocardiagram
recording of the electrical activity of the heart
(from the surface of the body)
fig 20-14
16
ECGs
different components
P wave QRS complex T wave
depolarization of the atria depolarization of
the ventricles bigger stronger
signal repolarization of the ventricles
17
ECGs
fig 20-14 EKG
18
ECGs
to analyze
size of voltage changes duration of
changes timing of changes
intervals
19
ECGs
fig 20-14 EKG
20
ECGs
intervals
P-R interval
from start of atrial depolarization to start of
QRS complex
time for signal to get from atrium to ventricles
if longer than 200 msec can mean damage to
conducting system
21
ECGs
intervals
Q-T interval
time for ventricular depolarization and
repolarization (ventricular systole)
if lengthened, may indicate, ion disturbances,
medications, conducting problems, ischemia, or
myocardial damage.
22
ECGs
intervals
T-P interval
from end of ventricular repolarization to start
of next atrial depolarization
the time the heart is in diastole the
isoelectric line
23
fig 20-14 EKG
T-P interval
24
ECGs
intervals
abnormalities cardiac electrical activity
cardiac arrhythmias
some are not dangerous others indicate damage to
heart
25
100 keys (pg. 688)
The heart rate is normally established by cells
of the SA node, but that rate can be modified by
autonomic activity, hormones, and other factors.
From the SA node the stimulus is conducted to the
AV node, the AV bundle, the bundle branches, and
Purkinjie fibers before reaching the ventricular
muscle cells. The electrical events associated
with the heartbeat can be monitored in an
electrocardiagram (ECG).
26
Electrical activity of the heart cells
99 of heart is contractile cells similar to
skeletal muscle AP leads to Ca2 around
myofibrils Ca2 bind to troponin on thin
filaments initiates contraction
(cross-bridges)
but there are differences nature of AP location
of Ca2 storage duration of contraction
27
Electrical activity of the heart cells
The action potential
resting potential of heart cells
-90mV threshold is reached near intercalated
discs signal is AP in an adjacent cell (gap
junctions)
28
Electrical activity of the heart cells
The action potential
review skeletal muscle
fig. 20-15
29
Electrical activity of the heart cells
The action potential
once threshold is reached the action potential
proceeds in three steps.
30
Electrical activity of the heart cells
The action potential - step 1
rapid depolarization (like skeletal
muscle) Na into cell through
voltage-gated channels (fast channels)
31
Electrical activity of the heart cells
The action potential - step 2
the plateau Na channels close Ca2 channels
open for a long time (slow calcium
channels) Ca2 in balances Na pumped out
32
Electrical activity of the heart cells
The action potential - step 3
repolarization Ca2 channels begin closing slow
K channels begin opening K rushes out restoring
resting pot.
33
Electrical activity of the heart cells
The action potential - step 3
repolarization
Na channels are still inactive cell will not
respond to stimulus refractory period
34
fig. 20-15a
35
Electrical activity of the heart cells
The role of calcium
extracellular Ca2 enters cells during the
plateau phase (20) Ca2 entering triggers
release of Ca2 from sarcoplasmic
reticulum ... heart is highly sensitive to
changes in Ca2 of the ECF
36
Electrical activity of the heart cells
The role of calcium
in skeletal muscle, refractory period ended
before peak tension developed summation was
possible tetanus. in cardiac muscle
refractory period lasts until relaxation has
begun no summation no tetanus.
37
Clinical note Heart attacks
blockage of coronary vessels myocardium without
blood supply cells die (infarction) myo
cardial infarction (MI) heart attack
38
Clinical note Heart attacks
blockage of coronary vessels
due to CAD (coronary artery disease)
(plaque in vessel wall) blocked by clot
(thrombosis)
39
Clinical note Heart attacks
blockage of coronary vessels
as O2 levels fall, cardiac cells will
accumulate anaerobic enzymes die and release
enzymes
LDH SGOT CPK CK-MB
lactose dehydrogenase serum glutamic oxaloacetic
transaminase creatine phosphokinase cardiac
muscle creatine phosphokinase
40
to here 3/26 lec 31
41
Clinical note Heart attacks
anticoagulants (aspirin) clot-dissolving
enzymes quick treatment will help reduce damage
due to blockage
42
Clinical note Heart attacks
risk factors
smoking high blood pressure high blood
cholesterol high LDL diabetes male severe
emotional stress obesity genetic
predisposition sedentary lifestyle
any 2 more than doubles your risk of MI
43
The cardiac cycle
contraction (systole)
relax (diastole)
fluid (blood) moves always moves from higher
pressure toward lower pressure
44
fig. 20-16
45
The cardiac cycle
atrial systole atrial diastole ventricular
systole ventricular diastole
generic heart rate 75 bpm
46
fig. 20-17
47
The cardiac cycle
atrial systole (100 msec)
blood in atria is pushed through AV valves into
ventricles tops off the ventricles blood in
ventricles is called EDV (end diastolic volume)
12
(follows path of least resistance)
end of atrial systole ventricular diastole begins
3
48
The cardiac cycle
ventricular systole (270 msec)
pressure start to rise in ventricle when it is
greater than pressure in atria, the AV valves
will close (chordae tendineae and papillary m.)
3
lubb
pressure continues to build until it can force
open the semilunar valves
4
49
The cardiac cycle
ventricular systole (270 msec)
up until now, ventricles have been contracting
but no blood has flowed isovolumetric
contraction
4
ventricular volume has not changed but the
pressure has increased
50
The cardiac cycle
ventricular systole (270 msec)
when pressure in ventricle is greater than
pressure in the arteries, the semilunar valves
will open
5
ventricular ejection
stroke volume
some blood left behind end systolic volume (ESV)
51
The cardiac cycle
ventricular systole (270 msec)
as pressure drops below that of arteries, the
semilunar valves will close again
6
Dupp
52
The cardiac cycle
ventricular diasatole (430 msec)
semilunar valves are shut AV valves are shut too
(temporarily) isovolumetric relaxation
7
when pressure gets below atrial pressure, AV
valves will open and ventricle will begin to fill
passively
8
53
fig. 20-17
54
Heart sounds
auscultation
stethoscope
lubb
DUPP
55
Heart sounds
lubb
closing of the AV valves as ventricular
contraction begins
56
Heart sounds
DUPP
closing of the semilunar valves as ventricular
relaxation begins
57
Heart dynamics
cardiac output heart rate stroke volume
variation adjustments
58
Heart dynamics definitions
EDV end diastolic volume ESV end systolic
volume Stroke volume
ventricle is full beginning to contract ventricle
is done contracting (a little blood left
inside) SV EDV - ESV
59
Heart dynamics definitions
cardiac output (CO) CO HR (heart rate) x
SV how much blood the heart pumps in a minute
both the SV and the HR can vary
60
Heart dynamics
both the SV and the HR can vary
fig. 20-20
61
Heart dynamics
variation in HR
autonomics dual innervation to SA node
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Heart dynamics HR
parasympathetics
releases ACh opens K channels lowers the
resting potential (hyperpolarize
cell) slows heart rate
controlled by cardioinhibitory centers in the
medulla oblongatat
63
Heart dynamics HR
parasympathetics
controlled by cardioinhibitory centers in the
medulla oblongata
reflexes hypothalamus
64
Normal
Parasympathetics
fig 20-22
65
Heart dynamics HR
sympathetics
releases NE binds to beta-1 receptors opens
Na/Ca2 channels depolarize cell speeds
up heart rate
66
Heart dynamics HR
sympathetics
controlled by cardioacceleratory centers in the
medulla oblongata
reflexes hypothalamus
67
Normal
Sympathetics
fig 20-22
68
Heart dynamics HR
atrial (Bainbridge) reflex
increased venous return stretches
atria stimulates stretch receptors stimulates
sympathetics increase HR (and CO)
69
Heart dynamics HR
hormones
E, NE, thyoid hormone affect SA node speed up
HR
70
to here 3/30/07 lec 33
71
Heart dynamics
stroke volume (SV)
remember SV EDV - ESV
72
Heart dynamics SV
EDV
the amount of blood in the ventricle at the end
of its diastolic phase, just before contraction
begins.
73
Heart dynamics SV
EDV
affected by the filling time venous return
preload
74
Heart dynamics SV
EDV
preload
the degree of stretching of the ventricle during
diastole
preload is proportional to EDV
affects heart muscles ability to generate tension
preload
75
Heart dynamics SV
EDV
preload
76
Heart dynamics SV
EDV
preload
more in more out
Frank-Starling principle
77
fig. 20-23
78
Heart dynamics SV
ESV
preload contractility afterload
79
Heart dynamics SV
ESV
contractility
amount of force generated with a contraction
increase decrease
inotropic action - inotropic action
80
Heart dynamics SV
ESV
contractility
factors that influence ANS hormones
81
Heart dynamics SV
sympathetic NS
NE, E
ESV
inotropic effect
contractility
ANS
parasympathetic NS
ACh
- inotropic effect
82
fig. 20-23
83
Heart dynamics SV
NE, E, glucagon, thyroid hormones
ESV
contractility
dopamine, dobutamine isoproterenol digitalis
hormones (and drugs)
inotropic effect
84
(hypertension)
Heart dynamics SV
propanolol timolol etc., (beta-blockers)
ESV
contractility
hormones (and drugs)
verapamil nifedipine (Ca2 blocker)
- inotropic effect
85
fig. 20-23
86
Heart dynamics SV
ESV
preload contractility afterload
the amount of tension needed to open semilunar
valves and eject blood
87
Heart dynamics SV
ESV
afterload
the amount of tension needed to open semilunar
valves and eject blood
greater afterload longer isovolumetric
contraction less ejected, larger ESV
88
Heart dynamics SV
ESV
afterload
restrict blood flow constrict peripheral
vessels circulatory blockage
inc. afterload
89
fig. 20-23
90
Summary
hormones venous return filling time venous
return preload contractility afterload
Heart rate EDV ESV SV EDV-ESV
91
100 keys (pg. 703)
Cardiac output is the amount of blood pumped by
the left ventricle each minute. It is adjusted
on a moment-to-moment basis by the ANS, and in
response to circulating hormones, changes in
blood volume, and alternation in venous return.
Most healthy people can increase cardiac output
by 300-500 percent.