Transcript Cardiac

Cardiac Physiology
Mechanical
Anatomy
Chambers
Blood
Cardiac
Heart
Pathology
Extrinsic
Electrocardiography
Valves
Flow
Physiology
Muscle
Control
of
of
ofThrough
to
Events
the
Intrinsic
the
the
heart
Heart
of
Heart
during
the
the
Conductance
Heart
Heart
Heart Contraction
System
Pericardium
Location:
Myocardium:
Heart
E.Atrioventricular
Semilunar
requires
(SL)
its
own
valves:
circulatory
Two:
Aortic:
system.
Between
MyocarTwo
circuits:
1.
Pulmonary:
side
of
the
heart
+begins,
3.
Ventricular
systole:
bundle
As
contraction
(ofRight
His):
Functional
intraEvents:
Events
Na+
influx
(slow)
offset
by
K
efflux
(slow),
Veins
Characteristics
of
right
Layers
atrium:
of
the
heart
Ventricles:
2.
4.
Isovolumetric
Systemic:
1.
left
Blood
side
relaxation:
leaving
of
the
heart
the
Occurs
heart,
during
2.
Most
early
of
3.
Work
loads
Four
chambers:
Two
atria
&
two
ventricles,
heart
dium
left
ventricle
is
too
thick
&
aorta
to
permit
&
pulmonary:Between
diffusion.
Coronary
right
cir+
+
1.
Fibrous
pericardium:
Tense
connective
tissue,
passage
ventricular
of
impulse
BP
increase(AV
from
atria
valves
to
ventricles
close,
semilunar
(no
gap
A.
C.
Atrioventricular
Left
AV
valve:Bicuspid:Mitral
(AV)
valves
valve:Two
cusps
a.
Blood
to
lungs
for
gas
exchange
K
1.
Start
permeability
point:
Atria
gradually
&
ventricles
decreases,
are
relaxed
Influx
of
(midNa
Cardiac
Angina
Intrinsic
5.
Electrical
Intervals
Purkinje
pectoris:
veins:
conduction
changes
fibers:
Follow
Temporary
during
Reach
system:
course
apex
heart
Noncontractile
deficient
of
then
activity
coronary
branch
blood
(ECG):
arteries,
superflow
cardto
Within
a.
Cardiac
mediastinun
muscle
arranged
of
medial
insurface,
cavity
circular
ofleft:
bundles
thorax,
1.
Branched,
short,
and
interconnected
fibers
Arrhythmias:
Uncoordinated
contractions
B.
mass
diastole,
of
heart,
T
wave,
right:
ventricles
anterior
relax,
intraventricular
inferior
Veins
Location
2.Atrioventricular
Cardiac
of
left
cycle
of
autorhythmic
atrium
(AV)
node:
cells
Depolarization
wave
is
divided
longitudinally:
Interatrial
&
interventrBrain-based
control
a.
Equal
volumes
culation:
ventricle
Arterial
&
pulmonary
supply:
trunk.
Right
Open
&
left
during
coronary
ventrprotects
heart,
anchors
heart
to
surrounding
Contraction
Autorhythmic
fibers:
Pace
maker
cells:
1%
of
Superior
vena
1.
Three
cava:
layers
Return
flow
from
regions
junctions
valves
closed),isovolumetric
between
cells
inatrium
atria
contraction
&
ventricles),
phase“vol1.
D.
Valves
Chordae
at
atrium-ventricular
tendineae
(heart
strings):
junction
Collagen
a.
Left
atrium
to
left
ventricle
depolarizes
to-late
diastole)
cardiac
cells,
Depolarization
opens
fast
join
myocardium,
iac
iorly
Deflection
P-R:
cells
to
into
form
Interval
that
ventricular
waves
coronary
initiate
thoracic
from
&
walls,
beginning
sinus
pain
distribute
is
impulses
to
symptom
empty
of
impulses
atrial
in
into
fibers
excitation
right
from
b.
Right
ventricle
to
left
of
the
heart
anterior
to
vertebral
column,
posterior
to
sternum,
2.
Striated
Fibrillation:
Rapid,
irregular
contractions
surface,
pressure
3.
drops,
Muscles:
Bd
in
Trabeculae
vessels
outside
carneae
heart
(crossbegins
1.
initiated
Systole
Sinoatrial
(contraction)
by
SA
(SA)
node
node:
reaches
&
diastole
Pacemaker:
AV
(relaxation),
node,
Fastest
AV
node
rate
is
of
b.
Unequal
work
loads
icular
septa,
atria
receive
returning
blood
(i.e.,
Cardioaccelatory
center
in
medulla,
sympathetic
b.
arteries
Fibrous
contraction
(arise
skeleton:
at
base
(systole):
Holds
of
aorta).
cardiac
Intraventricular
Left:
muscle
(supplies
together
pressleft
2+
2+
tissues,
prevents
over
filling
1.
heart
All
cardiac
muscle,
muscle
depolarize
cells
spontaneously
contract
as
a
single
unit
superior
to
diaphragm
Located
ume
constant”
in
inferior
(BP
in
interatrial
aorta&pulm.
septum,
trunk
very
exceeds
short
2.
cords
Prevent
attached
backflow
to
cusps,
into
anchor
atria
cusps
to
papillary
Four
pulmonary
veins:
Lungs
back
to
heart,
most
Ca
Ventricular
channels,
filling:
Ca
influx
Mid-to-late
from
ECS
diastole,
causes
AV
rising
atrium.
Myocardial
atria
moves
1.
&ventricular
P
wave:
to
faster
ventricles.
Tributaries:
Depolarization
infarction
than
excitation,
cell
Autorhythmic,
Great,
to
(MI):
(includes:
cell
moving
middle
Heart
contact
unstable
from
atrial
attack,
&
(ensures
small
SA
depolarizCardiac
RMP:
node
cardiac
superior
to
diaphragm
(at
rest),
superior
margin
3.
Cardiac
muscle
a.
Epicardium
fibers
are
functionally
connected
Ectopic
focus:
Excitable
tissue
other
than
SA
node
c.
Blood
returns
from
body
to
right
atrium,
low
O2
bars),
b.
to
Left
flow
papillary
ventricle
back
into
muscles
into
ventricles
aorta
(valve
(semilunar
function,
valves
project
close,
depolarization,
located
Length:
in
Total
interatrial
0.8
characteristic
s,
atrial
septum
systole
near
(sinus)
0.1
tricuspid
s,
rhythm.
ventricular
valve,
veins),
auricles
are
appendages
to
increase
atrial
NS
control,
innervate
SA
and
AV
nodes
side
ure
exceeds
of
heart
BP
by
in
marginal
aorta
&
branches:
pulmonary
anterior
trunk.
interThree
c.
Systemic:
Five
times
as
much
resistance
to
blood
+
2.
Contractile
Self-excitable
muscle
(
i.e.,
fibers:
autorhytmic):
Depolarize
Initiate
in
response
APs,
to
(branches
intraventricular
to
form
pressure,
bundle
branches)
pr.
in
ven.
increases
3.
muscles
Closed
during
during
ventricular
ventricular
contraction,
contraction
intraventr(systole)
of
the
posterior
surface
of
the
heart
phase
valves
of
are
AP,
open,
Repolarization
semilunar
valves
increases
are
closed,
K
permeabventveins.
cells
Drift
greater
through
ation
are
towards
&
Anterior
pumping
contraction,
atria
amitotic,
threshold.
cardiac
efficacy)
O2
passage
deficiency
veins
Pacemaker
of
empty
impulse
causes
potentials:
directly
necrosis
through
into
concentration,
relatively
high
CO2
concentration
(2nd
Endocardium:
rib),
inferior
margin
(5th
intercostal
space),
2.
Serous
pericardium:
Parietal
layer
(Internal
b.
(intercalated
Inferior
vena
discs,
cava:
desmosomes,
Return
flow
electrical
from
regions
coupling
controls
heart
contractions
into
aortic
heart
pr.
Increases
cavity),
4.
“dicrotic
Pulmonary
notch”),
trunk:
AV
Right
valves
still
Located
dia.
systole
of
fibers
0.3
in
s
right
&
is
quiescent
smaller
atrial
wall,
(slows
period
after
impulse
0.4
depolarization
s
conduction
is
volume,
fossa
ovalis
is
residual
impression
of
fetal
2.Cardioinhibitory
center,
X
nerve,
parasympatheflow,
longer
route
ventricular
crescent
shaped
&
circumflex
cusps
open
arteries).
against
Right:
arterial
(supplies
walls.
+
independent
pacemaker
cell
of
nervous
activities
innervation
b.
Middle
myocardium
4.
without
Bundle
volume
branches:
changing),
Course
ven.
interventricular
ejection
phase
B.
icular
Right
pressure
AV
valve:
rises
tricuspid:
forces
blood
Three
against
cusps
valve
c.
Aorta
to
body
through
systemic
arteries:
Gases
ility
ricles
(cardiac
begin
to
cells
fill
(70%
repolarize),
occurs
K
prior
channels
to
atrial
contright
(cell
Membrane
2.
intrinsic
QRS
death),
atrium.
complex:
conduction
potential
dead
Ventricular
cells
system),
changes
are
replaced
lasts
depolarization:
spontaneously
0.16
by
noncontras
60%
of
mass
to
the
left
of
midline,
base
(posterior
surface
of
fibrous
pericardium),
Visceral
layer
inferior
via
gap
junctions)
to
diaphragm
Heart
block:
Damage
to
AV
node:
Impulse
cannot
d.
Rt.
Atrium
to
right
ventricle
ventricle,
closed
(isovolumetric
routes
blood
relaxation)
to
lungs,
5.
Aorta:
Left
initiated,
‘0.1
s’
&
permits
depolarization
completion
wave
of
sweeps
atrial
contraction),
via
gap
foramen
ovale
tic
system,
innervate
SA
&
AV
nodes,
slows
HR
a.
right
F.
Inner
No
side
valves
myocardial
of
between
heart:
Marginal
surface
atria
&
&
venae
posterior
cavae
interven&
pulm3.
Long
refractory
period:
No
tetanic
contractions
septum
(intraventr.
toward
pressure
apex
of
exceeds
heart
pressure
in
large
(reinforced
flaps,
chordae
endocardium)
tendinea
anchor
flaps
in
closed
and
nutrients
are
exchanged
inactivate,
raction),
atrial
Cycle
systole
starts
(atria
again
contract
“preceded
by
ctile
Precedes
2.
Q-T:
scar
Ventricular
contraction
tissue.
depolarization
through
repolad.
Left
ventricle
is
much
larger
&
thicker
to
do
surface)
faces
right
shoulder,
apex
points
inferiorly
(epicardium:
part
of
heart
wall)
4.
Functional
c.
syncytium:
Deep
endocardium
Entire
myocardium
acts
reach
ventricles
ventricle,
5.
AV
valves
systemic
open
when
circulation
pr.
in
atria
exceeds
pr.
junctions
impulse
passes
throughout
to
bundle
atria
of
His
e.
Rt.
Ventricle
lungs:
Take
O2
&
give
CO2,
tricular
onary
veins
arteries).
.
Atrial
Anastomoses:
contraction
compresses
Collateral
routes
venous
c.
Coronary
sinus:
Drain
blood
from
myocardium
vessels,
semilunar
valves
open,
Bd
is
propelled
out
postion
more
work
P
wave”,
increased
atrial
pressure
propels
Bd
from
3.
rization,
T
wave:
includes:
Ventr.
repolarization,
time
of
ventricular
occurs
contraction
slower
than
toward
b.
Lines
left
heart
hip
&
(contacts
connective
chest
tissues
wall
of
between
valves
5th
as
a
single
unit
(result
of
gap
junctions)
pulmonary
arteries
(away
from
heart,
not
CO2)
d.
against
Systemic
AV
valves
veins
to
exerted
right
atrium
by
Bd
in
ventricles:
Start
of
entry
blood
points
flow.
Flow
occurs
only
during
diastole.
3.
Pericardial
cavity:
Between
serous
layers,
fluid
ventricles)
&PMI-point
atria begin
toout
fill&
with
blood
atria
intoribs
ventricles),
atria
relax
ventricles
depolarization:
more
spread
than
QRS
and
6th
&
of
maximum
intensity)
of
cycle,
quiescent
period
f.
Lungs
to
left
atrium:
Pulmonary
veins,
O2 rich
c.
Squamous
epithelium
filled
to
reduces
friction
between
serous
membr.s
Home
Exit
depolarize
(QRS
wave)
BASIM ZWAIN LECTURE NOTES
Cardiac Physiology
Cardiac
Heart
Sounds
Rate
Output
regulation
(CO)
Autonomic
system
Factors thatnervous
affect stroke
volume
Associated
Amount
of with
Bd pumped
closing by
of heart
each ventricle
valves: Lub-duppper min.=
1.
Sympathetic
nervous
system:
Responds
to real or
Preload-degree
of
stretch
prior
to
contraction
Chemical
Physical
factors
regulation:
3.
Parasympathetic
Opposes
sym.
NSclose,
(
pause
Stroke
lub-dupp-pause,
volume X HRdivision:
(SV=
…Sound
volume
1ven.
(AV
of Bd
valves
pumped
3.
Afterload-arterial
BP:
Pr.
that
contraction
perceived
threats:
Flight,
fright,
fight
and sex
CO
is
homeostatically
regulated:
Extrinsic
factors
(most
important
+ve
factor
affecting
EDV),
factors
1.
Age:
Hormones:
Inverse
Adrenal
relation
medulla
(Epinephrine
‘sym.
decreases
HR),
mediated
by
acetycholine
(hyperpoonset
out
ofovercome
of
each
systole,
ventricle
louder
per
&beat).
longer
CO
than
increase
sound
or
2),
must
(back
pr.
in
aorta
&
pul.
valves),
2.
Sympathetic
postganglionic
neurons
release
NE
induce
change
to
cardiac
function
through:
increasing
stretch:
vol.,
speed
of
venous
return
&
NS’
Gender:
increases
Female
HR
and
faster
contractility
‘like
NE’)
larizes
‘inhibits’
SA
node)
sound
decrease
2 (semilunar
with
SV or(aorta)
valves
HR, ..close,
SV=
beginning
EDV- ESV
oftrunk)
ventnormal:
80
mmHg
&
10
mmHg
(pul.
2+
at
cardiac
targets
(mediated
by
ß1exercise,
adr.
receptors:
a.
Neural
mechanisms
HR
(time
for
filling)
2.
3.
Ions:
Exercise:
Ca
Increased
conc.
(decrease
HR
during
causes
depressed
resting
ht
4.
Vagal
tone:
Sym.
&
parasym.
divisions
are
ricular
EDV
(end
diastole,
diastolic
short,
volume)
sharp
issound),
determined
pauseby (may
length
,pacemaker
not
normally
a
factor
in
healthy
individuals
cell
RMP
is brought
closer
tostrength
threshold
b.
Chemical
mechanisms
2.
Contractility:
Increase
in
contractile
(
function
rate
is
lower
&
increase
(bradycardia,
causes
ht
SV
irritability
&
muscle
mass
continuously
active
(effect
of
parasym.
division
(quiescent
of
ven.
diastole
period).
&effect
venous
Sounds
pr.of(120
separate
ml) subjects)
valves
can
have
an
adverse
in
hypertensive
2+
2+
‘depolarized’
&
increased
HR)
&
increases
Ca
c.
Physical
mechanisms
independent
of &
muscle
stretch),
increase
Caactivity
into
increased
in
athlete)
predominates)
dominant
effect
=
reduce
be differentiated:
ESV
(end systolic Timing
volume)(Mitral-Tricuspid-Aortic
is determined by arterial
influx
into
contractile
cells
(increases
ESV)
cardiac
cells
(increases
contractility
&
vol.
ejected
4.
Body
temperature:
HR
lowered
when
cold
of
AV
node
(25
beats/min
reduction
in
HR)
-Pulmonary)
pr.
& Force of&ven.
location
contraction
(four corners)
(50 ml)
from heart), decreased ESV, molecular regulation
ofExit
contractile events
Home
BASIM ZWAIN LECTURE NOTES