FUNCTION OF THE HEART AS A PUMP
By DR QAZI IMTIAZ RASOOL
1. Illustrate and discuss the action potential of contractile
cardiac fibers.
2. Describe the excitability changes during cardiac action
potential.
3. Describe excitation-contraction coupling of the cardiac
muscle.
4. Describe the intrinsic regulation of the cardiac pumping.
5. Describe the effect of various extrinsic factors on cardiac
pumping (nervous, physical and chemical).
Cardiovascular system
CARDIAC
MUSCLE
Intercalated discs
Latticework,
SYNCYTIUM
1.Atrial
2.Ventricle
AV bundle
Contractile cells
99%
Auto rhythmic
cells
1%
Sk. M.
Cardiac Channels
1.Leak K+ channel
2.Voltage-gated Channels
a) Na+ (INa)
b) Ca2+ (L-type; T-type) ICa,L
and ICa,T L channel or DHPR
dihydropyridine)
c) voltage-gated K+
delayed rectifier K+ channel
(rapid,slow,transient outward)
IKR, IKS, ITO)
d)Both Na+ /k/ca ("funny“)IF
e)Transporter
Na+/Ca2+ exchanger INCX
heart cell
1.
Phase 0 = Depolarization
2.
Phase 1 = Partial Rapid
Repolarization
3.
Phase 2 = Plateau
4.
Phase 3 = Repolarization
5.
Phase 4 = Resting Membrane
Potential
1.At threshold, voltage
gated Na++ channels open,
upstroke depend entirely on
it.
2. Na++ ions rush in.
RMP changes from -85mV
to+ 20mV.
“Fast” Na+ Current
Na+ current ends
Outward K+
current
It is small but fast repolarization.
1. Inactivation of Na+ channels ends
2. It is caused by Cl- influx
3. Transient outward K+ current channel KTO
1. Opening of the slow Ca2+- Na+ channels
leading to slow Ca2+ and Na+ influx. (Ltype calcium channels)
2. Delayed closure of the fast Na+ channels.
3.
permeability of K+ channels at the onset
of action potential leading to
K+ efflux
and consequently delayed repolarization.
Ventricular contraction persists throughout the action potential, so the long
plateau produces a long action potential to ensure forceful contraction of
substantial duration
RYR
DPHR
PLB
Phase 3
Outward K+
current--------repolarization
Na+ channel
recovery begins
during Relative
Refractory
Period by
closing and
become
refractory
= Outward K+ Current
Na+ Channel
Recovery
Na+ Channel
Configuration
Change
NOTE;_ Depolarization triggers
opening of voltage-gated potassium
ion channels.
.
Absolute refractory period (ARP)
1. During this period, the excitability of the cardiac muscle is
completely lost.
2. No other stimulus, whatever its strength can excite the cardiac
muscle.
3. It
coincides
(corresponds)
with:
the
phase
of
rapid
depolarization and the repolarization till the end of plateau (=
during systole of cardiac muscle).
NOTE;- Due to this long ARP, tetanus cannot be produced
in cardiac muscle. It is fatal because the heart as a pump
must contract and relax to fill with blood.
Na+
In
Cell
Excess Ca++
ions from CICR
ECF
Ca++
Out
Excess Ca++ ions from actinmyosin dissociation

RMP
1. When
membrane
potential comes to the
resting level.
2.
Na-K pump works to
derive excess Na+ out
and excess K+ in.
3. RMP remains stable
till it is excited again
1. Na+,K+-ATPase
2. Na+-Ca++ Exchanger
3. ATP-driven Ca++ Pump
Excitation-Contraction Coupling
Heart requires extracellular Ca ++ to contract.
1. i different --skeletal muscle, which contract in absence of Ca ++.
2.Long AP in cardiac muscle -- slow ---L-type Ca ++ channel --- sarcolemma.
3. Ca ++ coming into the cardiac muscle-- small and serves as a trigger
Local Currents depolarize adjacent channels causing
depolarization and opening of adjacent Na channels
Intrinsic Regulation of Heart Pumping—The Frank-Starling Mechanism
“Within physiologic limits greater the heart muscle is stretched during filling, the
greater is the force of contraction and the greater the quantity of blood pumped
into the aorta.”
Mechanism?
1.extra amount flows into the ventricles,
the cardiac muscle itself is stretched to
greater length.
- in turn causes the muscle to contract
with increased force because the actin
and myosin filaments are optimal
degree of overlap.
2. IF volume is increased. Stretch of the
right atrial wall directly increases the
heart rate by 10 to 20 percent;
although its contribution is much less
than that of the Frank-Starling
mechanism
Increases in atrial pressure causes an increase volume and strength of
contraction which causes an increase in cardiac output.
1.
2.
Slow heartbeat and exercise increase venous return to
the heart, increasing SV
Blood loss and extremely rapid heartbeat decrease SV
Extrinsic Factors
(drugs)
Hormones - thyroxine)+
Ca2 and some Intraand extracellular ion
concentrations
1. Contractility – cardiac cell
contractile force due to
factors other than EDV
2. Preload – amount ventricles
are stretched by contained
blood – EDV
Stroke volume
Strength of
cardiac contraction
3. Venous return - skeletal,
respiratory pumping
End-diastolic
volume
4. Afterload – back pressure
exerted by blood in the large
arteries leaving the heart
Venous return
Effect of ANS+DRUGS
Effect of K+AND Ca++
1. K+AND Ca++
-
Excess causes effects opposite to those of K+, causing spastic contraction.
-Deficiency causes cardiac flaccidity, similar to the effect of high potassium.
Fortunately, calcium ion levels in the blood normally are regulated within a very
narrow range.
NOTE;- cardiac effects of abnormal calcium concentrations are seldom of
clinical concern.
2. Temperature
- Increased(fever)- increased heart rate,
-Decreased – decreased ( hypothermia 60° to 70°F).
Mechanism:- 1.heat ↑ permeability of the cardiac muscle membrane to ions
that control heart rate
2.Contractile strength temporarily by a moderate increase, but
prolonged elevation exhausts the metabolic systems of the heart and eventually
causes weakness.
3. Hypernatremia–
-blocks
heart contraction by inhibiting ionic calcium
transport ????????