Brief overview of cardiac physiology

1. Cardiovascular Anatomy and
Physiology

2. Cardiovascular Anatomy
•Weighs between 200-400 grams
•By the end of a normal life it may have beat more than 3.5
billion times
•Each day the heart beats 100,000 times
•Pumping about 7,751 litres of blood.

3. Cardiovascular Anatomy
•Located between lungs
•Behind and slightly to the left
of sternum
•Double layered membrane
called pericardium surrounds
heart
•Outer layer of pericardium
attached by ligaments to
spinal column and diaphragm
•Coating of fluid separates
the two membranes

4. Cardiovascular AnatomySuperior vena cava takes
deoxygenated blood from
body
Pulmonary artery sends
deoxygenated blood to the
lungs
Pulmonary veins
take oxygenated
blood from the lungs
Inferior vena cava takes
deoxygenated blood from
body
Aorta sends
oxygenated blood
around the body

5. Cardiovascular Anatomy
The tricuspid valve regulates blood flow
between the right atrium and right ventricle.
The mitral valve lets oxygen-rich
blood from your lungs pass from the
left atrium into the left ventricle.

6. Cardiovascular Anatomy
The pulmonary valve controls blood flow
from the right ventricle into the pulmonary
arteries, which carry blood to your lungs to
pick up oxygen.
The aortic valve opens the way for
oxygen-rich blood to pass from the
left ventricle into the aorta, your
body's largest artery, where it is
delivered to the rest of the body.

7. Cardiovascular Anatomy

8. Cardiovascular Anatomy

9. Cardiac muscle
•Contractile
proteins
•Contraction
achieved through
release of calcium
•Rich in
mitochondria-
aerobic
dependent
•Fibres connect to
each other
through
intercalcated
discs

10. Action Potentials
Resting membrane
potential -90mV
Rapid
depolarisation to
+20mV
Partial repolarisation to
5-10mV
Slow
Repolarisation
Rapid
repolarisation

11. Action Potentials
Cardiac cells absolutely refractory to
stimulation for whole duration of action
potential
Second action potential
cannot be generated for up
to 350ms
Prolonged action potential
protects against pump
failure caused by sustained
contraction
Sets upper rate of
contraction 3-4 beats per
second.

12. Membrane potential
Depolarisation opens sodium
channels
Inward sodium current causes
further depolarisation
Calcium channels open more
slowly
Once open keeps membrane
depolarised and maintains
plateau.
Initially less outward flow of
Potassium
Then outward flow increases repolarising the
membrane

13. Membrane potential
Rapid depolarisation
Sodium rushes in
Calcium inflow
slower
Maintains plateau
Potassium outflow
reduced, then rises
This repolarises
membrane

14. Automaticity
• Action potentials are generated
spontaneously within the cells
themselves- myogenic.
• Known as pacemaker cells
• Instead of constant resting potential
there is a steady depolarising
potential
• Once action potential is generated at
one site it is rapidly conducted.
• Driven by fastest pacemaker cells in
heart- normally SA node.

15. Conducting pathways in the Heart
AP’s conducted away from SA node by atrial
fibres.
Made possible by low resistance junction at
intercalcated discs
Produces atrial contraction
AV node capable of pacemaker activity but
normally driven by SA node.
Slow conduction which ensures ventricular
contraction does not take place until atrial
contraction complete.
Action potential travels down left and right side
of Bundle of His
Transmission through Bundle and Purkinje
fibres rapid to promote synchronised
contraction of ventricles.

16. Cardiac Cycle- Ventricular pressure
During ventricular diastole
ventricular pressure is low-
1mmHg
Rises to about 5mmHg at end
of atrial systole as blood is
forced into ventricle.
Ventricular systole
commences raising
pressures rapidly to about
120mmHg
Peak pressure in right
ventricle about 25mmHg
As heart rate increases
diastole shortens.
Inadequate filling in short
diastole compromises heart
if heart rate too high.

17. Cardiac Cycle- Atrial pressure
Atrial pressure remains constant at
about 1mmHg until....
Atrial systole when pressure rises
to about 6mmHg
This is the a wave.
Atrium relaxes and AV valve closes
(mitral valve, tricuspid valve)
Causes back pressure on valve
cusps.
Rise in pressure results in c wave.
Aortic and pulmonary valves open
and atrial pressure falls to almost
zero.
Blood enters atria from venous
system.
AV valves are closed so pressure
rises.
This is v wave

18. Cardiac Cycle- Aortic pressure
During ventricular diastole there is
a gradual decline in aortic pressure
to about 80mmHg
During this time aortic pressure
higher than ventricular pressure
so AV remains closed
During systole ventricular
pressure rises opening valve
Aortic pressure peaks at about
120mmHg
Pressure drops and aortic valve
closes causing small rise in
pressure.....
Dicrotic notch

19. Cardiac Cycle- Heart Sounds
First heart sound- lub-
caused by closure of
mitral and tricuspid
valves at start of systole
Second heart sound-
dub- caused by closure of
aortic and pulmonary
valves at end of systole

20. Ventricular Volume
At the end of systole there is
about 80mls of blood in
ventricle
This increases to about
130mls during diastole due
to passive filling from the
atrium
Active filling from the atrium
only increases this by about
25% to 150mls
Approximately 70mls of
blood ejected during systole
The dominant effect of passive filling
explains why ventricular filling is still possible
in the absence of coordinated atrial
contraction e.g. Atrial fibrillation

21. Cardiac Output
Cardiac output = heart rate X stroke volume
At rest:
Cardiac output = 70bpm X 70ml/beat
=
4900ml/min
Or
5 Litres per minute.

22. Intrinsic control of cardiac output
Increased force of
contraction as resting
length of cardiac muscles
increased
Results in increased
in increases in stroke
volume as volume of
ventricle immediately
before contraction
was increased

23. Intrinsic control of cardiac output
Preload-
Refers to level of stretch in a relaxed muscle just
before it contracts.
In the heart this is largely dictated by the venous
return.
So increased venous return increases stretch in
muscle which increases cardiac out put.
Afterload-
Refers to the force that the muscle must
generate during contraction.
Most affected by changes in arterial
pressure

24. Extrinsic control of cardiac output
•Nervous control
•Sympathetic
•Parasympathetic
•Can alter heart rate- chronotropic effects
•Can alter force of contractility- inotropic effects.

25. Extrinsic control of cardiac output
•Nervous control
•Sympathetic.
•Controlled in a number of regions of the CNS
•Postganglionic nerves release neurotransmitter noradrenaline
•Stimulation of nerves leads to
• increased heart rate (positive chronotropic effect)
•Increased myocardial contractility (positive inotropic effect)
•Leads to increased cardiac output at any given pressure
•Limits to benefits of increased heart rate due to compromised
atrial filling.

26. Extrinsic control of cardiac output
•Nervous control
•Parasympathetic.
•Come from medulla oblongata in the brain and reach heart via
vagus nerve.
•Supply SA and AV node and release acetylcholine when
stimulated
•This slows heart (negative chronotropic effect) through its
influence on pacemaker activity.
•Reduction in cardiac activity.

27. Extrinsic control of cardiac output
•Hormonal Control
•Catecholamines
•Adrenaline
•Noradrenaline
•Released by adrenal medullary cells in response to sympathetic
nervous stimulation
•Increase both heart rate and myocardial contractility

28. Pi Po
So there are only two ways in
which we can affect blood flow
Control of arterial pressure
For fluid to flow through a pipe there
must be a pressure gradient between
the two ends of that pipe.
The size of that gradient(arterial
pressure) equals the rate of
flow(cardiac output) times the
resistance to that flow(SVR).
OR Cardiac Output = Arterial Pressure X Resistance
Changing
pressure
difference
across its
vascular bed
Changing its
vascular
resistance

29. Control of arterial pressure
If Cardiac output is constant
then pressure difference
between two points will be
proportional to the
resistance.
Pressure in aorta and large
arteries is high and pulsatile
and there is only a small
drop in pressure along their
length.
Largest pressure drop occurs
in the arterioles
So single largest contribution
to peripheral resistance
comes from the arterioles
Therefore peripheral
resistance can be controlled
by constriction or dilation of
these vessels

30. Regulation of arterial pressure.
• Nervous control
– Vasomotor centre- activates sympathetic nerves;
• Stimulate heart rate and contractility
• Release noradrenaline
• Causes venules to constrict which increases venous
return, increasing cardiac output.
• Preganglionic sympathetic nerves stimulate release of
adrenaline and noradrenaline from adrenal medulla.

31. Regulation of arterial pressure.
• Nervous control
– Baroreceptor reflexes
• Stretch receptors in carotid sinus and aortic arch
• Increases in arterial pressure stretch aorta and carotid.
• This stimulates sensory output from receptors
• Which inhibits sympathetic outflow to the
cardiovascular system and...
• Stimulates parasympathetic nerves thereby...
• Reducing cardiac output.
• Respond very rapidly.

32. Regulation of arterial pressure.
• Nervous control
– Low pressure volume receptor reflexes
• In walls of great veins, atria and pulmonary trunk.
• Particularly sensitive to changes in blood volume
• Increased blood volume stretches these receptors....
• Which reduce blood pressure by...
• Reducing vasoconstrictor sympathetic activity, reducing
resistance..
• Release of ADH is inhibited
• ADH causes direct vasoconstriction and stimulates
water absorption from the kidney.

33. Regulation of arterial pressure.
• Nervous control
– Chemoreceptors
• Found in aortic and carotid bodies
• Sensitive to changes in tissue oxygen levels
• So if arterial pressure is very low oxygen levels may
drop at the tissue level
• Stimulate vasoconstrictor sympathetic nerves to
restore blood pressure.

34. Regulation of arterial pressure.
• Hormonal control
– Catecholamines
• Adrenaline/noradrenaline
– ADH (vasopressin)
• Vasoconstrictor
– Renin-angiotensin-aldosterone system.

35. Renin-angiotensin-aldosterone system.

36. Requirements for effective operation
• Contractions of cardiac muscle cells must occur at
regular intervals and be synchronized (not arrhythmic).
• Valves must be fully open (not stenotic)
• Valves must not leak (not insufficient or regurgitant)
• Muscle contractions must be forceful (not failing)
• Ventricles must fill adequately during diastole.