Download Heart Anatomy and Cardiac Muscle Cell Structure

Heart Anatomy and Cardiac Muscle Cell Structure
Chapter 12
Figure 12.1: Location of the Heart
Aorta
Vena
Cava
Pulmonary
Trunk
RA
RV
Right
Coronary
Artery
Fig 12.2: The Heart
 Figure 12.3: VentricularMusculature
Figure 12.4: A-V Valves
Figure 12.5. Aortic & Pulmonary Valves
Figure 12.6:
Pulmonary vein
SA NODE
Vena Cava
L
R
AORTA
AV NODE
AV
Bundle
&
Purkinje
Fibers
PULMONARY
ARTERY
Fig 12.8
Blood Flow
Systemic Capillaries --> Veins-->Vena Cava --> Right Atrium --> Right Ventricle
Pulmonary Artery --> Pulmonary Capillaries --> Pulmonary Vein
Left Atrium --> Left Ventricle --> Aorta --> Arteries --->Systemic Capillaries
Cardiac cell structure
 Small discrete cells
 Intercalated disks with desmosomes
 Gap junctions = syncytium
 Many mitochondria
 Sr and t tubules
 Striated
Figure 12.7: Cardiac Muscle Cells
Fig 12.8: Cardiac Conduction System
Electrical Activity of the Heart
Fig 12.10: Pacemaker Cell
Ion channels in pacemaker cells: see page 381
•
•
Slow initial depolarization caused by closing of K+ channels
Next funny channels open
– Allow Na to enter causing depolarization
– Only open briefly
+
•
This depolarization opens two types of Ca++ channels
-T - type channels open briefly before inactivating
- L - type channels then open finishing
depolarization
Note Differences in Conduction Velocity Due to Rates of Depolarization!
RECTIFICATION
Minimized efflux of K+ during AP plateau because of decreased K+ conductance at this
positive Vm
See Fig 12.10 !!!!


Duration for complete contraction of the ‘pump’
Long AP with long refractory period to prevent fibrillation
ACh or PARASYMP.
ON SA NODE
Vm
mV
- 60
Inc. P K
Dec. P Ca
ACh
See Fig 12.10 !!!!
SA NODE:
NE or EPI
Vm
mV
- 60
+ P Na
and P Ca
and - P K
SYMPATHETIC
STIMULATION
See Fig 12.10 !!!!
VENTRICULAR
ACTION POTENTIAL
Vm
in
mV
0
-80
F
O
R
C
E
0
0.1
0.2
SECONDS
0.3
Fig 12.12: Einthoven’s Triangle and the ECG: Figure 12.13
ECG
R
T
P
Q
S
M
U
S
C
L
E
F
O
R
C
E
POTENTIAL
ISOMETRIC
FOR CE
AFTERLOAD
ISOTON IC
SHORTENING
Systole
ISOMETRIC
R ELAXATION
ISOMETRIC
C ON TR ACTION
Diastole
MUSCLE LENGTH
Terminology
 End Systolic Volume (ESV in ml)
 End Diastolic Volume (EDV in ml))
 Stroke Volume (SV in ml/beat)
 SV = EDV - ESV
 Heart Rate (in beats/min)
 SV (ml/beat)
 Cardiac Output (CO in ml/min)
 CO = HR x SV
Starling’s Law of the Heart
Increased EDV or myocardial fiber length results in increased SV or increased strength of
contraction.
Basis for Starling’s Law:
P = 2T/r
where
P = pressure in ventricle or aorta at ejection
T = myocardial tension required to generate that tension
r = radius of ventricle at beginning of systole
P = 2T/r
Which ventricle must develop more tension or contractile force, a fuller, larger EDV or a
smaller EDV?
M
U
S
C
L
E
F
O
R
C
E
POTENTIAL
ISOMETRIC
FOR CE
ISOTON IC
SHORTENING
ISOMETRIC
R ELAXATION
AFTERLOAD
ISOMETRIC
C ON TR ACTION
Filling
MUSCLE LENGTH
Sympathetic response
 1 receptors on nodes and atrial and ventricular muscle cells
 Increases rate
 Increases ca++ released per beat via cyclic amp

1 receptor activation
 G protein  adenylate cyclase --> cyclic AMP
 Activates cAMP-dependent protein kinase
 Phosphorylates an SR protein, phospholamban
 myocardial SR takes up and releases more Ca++ per beat
result = more cross bridges = more tension
As heart rate increases,
filling time decreases
DIGITALIS
DECREASE HR
BUT
INCREASE STRENGTH
Vagus nerve
•Parasympathetic fibers
•Baroreceptors from aortic arch
•Stretch receptors from lungs
Parasympathetic nerves
Right vagus to SA node
Left vagus to AV node and bundle
Decreases rate
No DIRECT influence on strength
12 0
10 0
LEFT
HEART
80
b
60
VENTRICULAR
Press ure
40
AORTIC
Press ure
c
a - mitral closes
b - aortic opens
c - aortic closes
d - mitral opens
ATRIAL
Press ure
20
a
d
0
150
100
Ventricular
Volume in
mls
50
T IME: 0
0.1 sec
0.2
0.3
R
E
C
G
S
O
U
N
D
S
P
P
T
Q
4
S
1
2
3