PowerPoint presentation of the heart for pathological study

1. PHYSIOLOGY OF CARDIAC
MUSCLE

2. PHYSIOLOGICAL PROPERTIES OF CARDIAC
MUSCLE
• Excitability: ability to respond to an electrical impulse
• Excitation - the process of generation of action potential
• Excitability - the ability to generate an action potential
• Automaticity: ability to initiate an electrical impulse
• Conductivity: ability to transmit an electrical impulse from one cell to
another
• Contractility is a term used to denote the force generated by the
contracting myocardium under any given condition

3. The Heartbeat
• What Two Types of Cardiac Cells are Needed for
the Heartbeat?
•Contractile cells
•Provide the pumping action
•Cells of the conducting system
•Generate and spread the action potential

4. EXCITABILITY

5. Myocardial Physiology
Contractile Cells
•Special aspects
• Intercalated discs
• Highly convoluted and interdigitated junctions
• Joint adjacent cells with
• Desmosomes & fascia adherens
• Allow for synticial activity
• With gap junctions
• More mitochondria than skeletal muscle
• Less sarcoplasmic reticulum
• Ca2+ also influxes from ECF reducing storage
need
• Larger t-tubules
• Internally branching
• Myocardial contractions are graded!

6. Myocardial Physiology
Contractile Cells
• Special aspects
• The action potential of a contractile cell
• Ca2+ plays a major role again
• Action potential is longer in duration than a “normal” action potential due to
Ca2+ entry
• Phases
4 – resting membrane potential @ -90mV
0 – depolarization
• Due to gap junctions or conduction fiber action
• Voltage gated Na+ channels open… close at 20mV
1 – temporary repolarization
• Open K+ channels allow some K+ to leave the cell
2 – plateau phase
• Voltage gated Ca2+ channels are fully open (started during initial
depolarization)
3 – repolarization
• Ca2+ channels close and K+ permeability increases as slower activated
K+ channels open, causing a quick repolarization
• What is the significance of the plateau phase?

7. Myocardial Physiology
Contractile Cells
The action potential of a
contractile cell Ca2+ plays a
major role again
Action potential is longer in
duration than a “normal”
action potential due to
Ca2+ entry

8. Myocardial Physiology
Contractile Cells
Phases
4 – resting membrane
potential @ -90mV
The inward current that
balances this outward current
is carried by Na+ and Ca2+, even
though the conductances to
Na+ and Ca2+ are low at rest.

9. Myocardial Physiology
Contractile Cells
Phases
0 – depolarization
Due to gap junctions or
conduction fiber action
Voltage gated Na+ channels
open… close at 20mV

10. Myocardial Physiology
Contractile Cells
Phases
1 – temporary repolarization
Open K+ channels allow some
K+ to leave the cell

11. Myocardial Physiology
Contractile Cells
Phases
2 – plateau phase
Voltage gated Ca2+ channels
are fully open (started during
initial depolarization)

12. Myocardial Physiology
Contractile Cells
Phases
3 – repolarization
Ca2+ channels close and K+
permeability increases as
slower activated K+ channels
open, causing a quick
repolarization

13. Myocardial Physiology
Contractile Cells
Skeletal Action Potential vs Contractile
Myocardial Action Potential

14. Myocardial Physiology
Contractile Cells
• Plateau phase prevents summation due to the
elongated refractory period
• No summation capacity = no tetanus
• Which would be fatal

15. AUTOMATICITY
• property automatic - the ability to spontaneously excited

16. • SA node:
• Demonstrates automaticity:
• Functions as the
pacemaker.
• Spontaneous depolarization
(pacemaker potential):
• Spontaneous diffusion
caused by diffusion of
Ca2+ through slow Ca2+
channels.
• Cells do not maintain
a stable RMP.

17. Myocardial Physiology
Autorhythmic Cells (Pacemaker Cells)
•Characteristics of Pacemaker
Cells
• Smaller than contractile cells
• Don’t contain many myofibrils
• No organized sarcomere
structure
• do not contribute to the
contractile force of the heart
normal contractile myocardial
cell
conduction myofibers
SA node cell
AV node cells

18. Myocardial Physiology
Autorhythmic Cells (Pacemaker Cells)
• Characteristics of Pacemaker Cells
• Unstable membrane potential
• “bottoms out” at -60mV
• “drifts upward” to -40mV, forming a pacemaker potential
• Myogenic
• The upward “drift” allows the membrane to reach threshold potential (-40mV) by itself
• This is due to
1. Slow leakage of K+ out & faster leakage Na+ in
• Causes slow depolarization
• Occurs through If channels (f=funny) that open at negative membrane
potentials and start closing as membrane approaches threshold potential
2. Ca2+ channels opening as membrane approaches threshold
• At threshold additional Ca2+ ion channels open causing more rapid
depolarization
• These deactivate shortly after and
3. Slow K+ channels open as membrane depolarizes causing an
efflux of K+ and a repolarization of membrane

19. Myocardial Physiology
Autorhythmic Cells (Pacemaker Cells)
• Altering Activity of Pacemaker Cells
• Sympathetic activity
• NE and E increase If channel activity
• Binds to β1 adrenergic receptors which
activate cAMP and increase If channel
open time
• Causes more rapid pacemaker potential
and faster rate of action potentials
Sympathetic Activity Summary:
increased chronotropic effects
heart rate
increased dromotropic effects
conduction of APs
increased inotropic effects
contractility

20. Myocardial Physiology
Autorhythmic Cells (Pacemaker Cells)
• Altering Activity of Pacemaker Cells
• Parasympathetic activity
• ACh binds to muscarinic receptors
• Increases K+ permeability and decreases
Ca2+ permeability = hyperpolarizing the
membrane
• Longer time to threshold = slower rate
of action potentials
Parasympathetic Activity Summary:
decreased chronotropic effects
heart rate
decreased dromotropic effects
 conduction of APs
decreased inotropic effects
 contractility

21. Rhythm of Conduction System
•SA node fires spontaneously 90-100 times per minute
•AV node fires at 40-50 times per minute
•If both nodes are suppressed fibers in ventricles by
themselves fire only 20-40 times per minute
•Atrioventricular bundle of His
•Ventricular tissue fires at 20-40 beats/minute and can
occur at this point and down
•Artificial pacemaker needed if pace is too slow
•Extra beats forming at other sites are called ectopic
pacemakers
•caffeine & nicotine increase activity

22. Normal pacemaker activity
• various autorhythmic cells have different rates of depolarization to threshold –
so the rate of generating an AP differs
• AP propagated through gap junctions or through the conduction system of the
heart
• contraction rate is driven by the SA node – fastest autorhythmic tissue

23. blockage of transmission from SA through the AV node
failure of SA node

24. • in some cases – the normally slowest Purkinje fibers can become overexcited = ectopic focus
• premature APs
• premature ventricular contraction (PVC)
• occurs upon excess caffeine, alcohol, lack of sleep, anxiety and stress
• some organic conditions can also lead to this

25. Cardiac Conduction

26. Conducting Tissues of the Heart
•APs spread through myocardial cells through gap junctions.
•Impulses cannot spread to ventricles directly because of
fibrous tissue.
•Conduction pathway:
•SA node.
•AV node.
•Bundle of His.
•Purkinje fibers.
•Stimulation of Purkinje fibers cause both ventricles to
contract simultaneously.

27. Conduction System of Heart
• gap junctions – two PMs are connected by a “channel” made
of specific proteins = connexons
• connexons are 6 protein subunits that form a hollow tube-like
structure
• two connexons join end to end to connect the cells
• allow a free flow of materials from cell to cell
• allow for the spread of electricity within each atrium and
ventricle
• no gap junctions connect the atrial and ventricular contractile
cells – block to electrical conduction from atria to ventricle!!!
• also a fibrous skeleton the supports the valves –
nonconductive
• therefore a specialized conduction system must exist to allow
the spread of electricity from atria to ventricles

28. Intrinsic conduction system
1. Intrinsic conduction system
▪ Built into heart tissue & sets basic rhythm
▪ Pacemaker = Sinoatrial (SA) Node
Sequence of action:
1.Sinoatrial (SA) node – right atrium
• Generates impulses  Starts each heartbeat
2.Atrioventricular (AV) node – between atria & ventricles
• Atria contract
3.Bundle of His (or AV bundle)
4.Bundle branches – interventricular septum
5.Purkinje fibers – spread within ventricle walls
• Ventricles contract

30. Conduction of Impulse
•APs from SA node spread quickly at rate of 0.8
- 1.0 m/sec.
•Time delay occurs as impulses pass through AV
node.
• Slow conduction of 0.03 – 0.05 m/sec.
•Impulse conduction increases as spread to
Purkinje fibers at a velocity of 5.0 m/sec.
• Ventricular contraction begins 0.1–0.2 sec.
after contraction of the atria.

31. • atrial conduction
system/interatrial pathway –
spread of electricity from right
to left atrium ending in the LA
• through gap junctions of the
contractile cells

32. • internodal pathway – spread of
electricity to the AV node via
autorhythmic cells
• SA to AV node – 30msec
• BUT spreads relatively slowly
through the AV node
• this allows for complete filling
of the ventricles before they
are induced to contract = AV
nodal delay

33. • ventricular conduction system
(Purkinje system) – Bundles of His
and Purkinje fibers
• travel time = 30 msec
• PFs conduct impulse 6 times
faster than the ventricular muscle
cells would on their own
• the PFs do not connect with
every ventricular contractile cell
• so the impulse spreads via gap
junctions through the ventricle
muscle – similar to the atrial
system
• diffusion through the PFs allow
for simultaneous contraction of
all ventricular cells

34. Cardiac excitation
efficient cardiac function requires three criteria
• 1. atrial excitation and contraction should be complete before ventricular excitation and
contraction
• opening and closing of valves within the heart depend upon pressure – which is generated
by muscle contraction
• so simultaneous contractions of atria and ventricles would lead to permanent closure of
the AV valves – myocardium of the ventricles is larger and stronger
• normally – atrial excitation and contraction occurs about 160 msec before ventricular
• 2. cardiac fiber excitation should be coordinated to ensure each chamber contracts as a unit
• muscle fibers cannot become excited randomly
• role of the gap junctions
• 3. atria and ventricles should be functionally coordinated
• atria contract together, ventricles contract together
• permits efficient pumping of blood into the pulmonary and systemic circuits
• uncontrolled excitation and contraction of ventricular cells – fibrillation
• correction by:
• 1. electrical defibrillation
• 2. mechanical defibrillation

35. Electrocardiogram---ECG or EKG
• electrical currents generated by the heart
are also transmitted through the body
fluids
• can be measured on the surface of the
chest
• therefore it is not a direct measurement of
the actual electrical conductivity of the
heart itself
• represents the overall spread of activity
through the heart during depolarization –
sum of all electrical activity
• measured through the placement of 6
leads on the chest wall (V1 – V6) PLUS 6
limb leads (I, II, III, aVR, aVL and aVF)

36. Electrocardiogram---ECG or EKG
• it's usual to group the leads according to
which part of the left ventricle (LV) they
look at.
• AVL and I, as well as V5 and V6 are
lateral, while II, III and AVF are inferior.
• V1 through V4 tend to look at the
anterior aspect of the LV

37. Electrocardiogram---ECG or EKG
• P wave
• atrial depolarization
• SA depolarization is too weak to measure
• smaller than the QRS complex due to the smaller size
of the atrial muscle mass
• will be affected by abnormalities in the pacemaker
activity of the SA node
• PR segment/PQ interval – AV nodal delay
• P to Q interval
• conduction time from atrial to ventricular excitation
• no net current flow within the heart musculature &
the flow through the AV node is too small to
measure– baseline
• if activity in the AV node is abnormal – this interval ill
be affected

38. Electrocardiogram---ECG or EKG
• QRS complex
• ventricular depolarization
• will be affected by the appearance of an ectopic
focus (region of hyperactive ventricular contraction)
• ST segment – time during which ventricles are
contracting and emptying
• ventricles are completely depolarized and the cells
are in their plateau phase
• T wave
• ventricular repolarization
• TP interval
• time during which ventricles are relaxing and filling

39. CONTRACTILITY

40. Myocardial Physiology
Contractile Cells
• Initiation
• Action potential via pacemaker cells to conduction
fibers
• Excitation-Contraction Coupling
1. Starts with CICR (Ca2+ induced Ca2+ release)
• AP spreads along sarcolemma
• T-tubules contain voltage gated L-type Ca2+
channels which open upon depolarization
• Ca2+ entrance into myocardial cell and opens RyR
(ryanodine receptors) Ca2+ release channels
• Release of Ca2+ from SR causes a Ca2+ “spark”
• Multiple sparks form a Ca2+ signal

41. Myocardial Physiology
Contractile Cells
• Excitation-Contraction Coupling cont…
2. Ca2+ signal (Ca2+ from SR and ECF) binds to troponin
to initiate myosin head attachment to actin
• Contraction
• Same as skeletal muscle, but…
• Strength of contraction varies
• Sarcomeres are not “all or none” as it is in
skeletal muscle
• The response is graded!
• Low levels of cytosolic Ca2+ will not
activate as many myosin/actin
interactions and the opposite is true
• Length tension relationships exist
• Strongest contraction generated
when stretched between 80 &
100% of maximum (physiological
range)
• What causes stretching?
• The filling of chambers
with blood

42. Cardiac Cycle

43. Cardiac Cycle
Phases
•Systole = period of contraction
•Diastole = period of relaxation
•Cardiac Cycle is alternating periods of
systole and diastole

44. Cardiac cycle
• A. Midventricular diastole
• during most of the ventricular
diastole, the atrium is also in
diastole = TP interval on the EKG
• as the atrium fills during its
diastole, atrial pressure rises and
exceeds ventricular pressure (1)
• the AV valve opens in response to
this difference and blood flows
into the right ventricle
• the increase in ventricular volume
rises even before the onset of
atrial contraction (2)

45. Cardiac cycle
• B. Late ventricular diastole
• SA node reaches threshold and fires its impulse to the AV
node = P wave (3)
• atrial depolarization results in contraction – increases the
atrial pressure curve (4 – green line)
• corresponding rise in ventricular pressure (5 – red line)
occurs as the ventricle fills & ventricular volume increases
(6)
• the impulse travels through the AV node
• the atria continue to contract filling the ventricles
• C. End of ventricular diastole
• once filled the ventricle will start to contract and enter its
systole phase
• ventricular diastole ends at the onset of ventricular
contraction
• atrial contraction has also ended
• ventricular filling has completed
• ventricle is at its maximum volume (7) = end-diastolic
volume (EDV), 135ml

46. • D. Start of ventricular systole
• at the end of this contraction is the onset
of ventricular excitation (8) = QRS
complex
• the electrical impulse has left the AV
node and enters the ventricular
musculature
• this induces ventricular contraction
• ventricular pressure will begin to rise
rapidly after the QRS complex (red line)
• this increase signals the onset of
ventricular systole (9)
• atrial pressure is at its lowest point as its
contraction has ended and the chamber is
empty (green line)
• the ventricular pressure now exceeds
atrial – AV valve closes
Cardiac cycle

47. Cardiac cycle
• E. isovolumetric ventricular contraction
• ventricular pressure also opens the semilunar valves
• however, just after the closing of the AV and opening of the SL is a brief moment
where the ventricle is a closed chamber (10) = isovolumetric contraction
• ventricular pressure continues to rise (red line) but the volume within the
ventricle does not change (11)
• F. Ventricular ejection
• ventricular pressure will now exceed aortic pressure as the ventricle continues is
contraction (12)
• aortic SL is forced open and the ventricle empties
• this volume of blood – stroke volume (SV)
• the ejection of blood into the aorta increases its pressure (aortic pressure) and
the aortic pressure curve rises (13 – purple line)
• ventricular volume now decreases (14 – blue line)
• F. End of ventricular systole
• as the ventricular volume drops
• BUT ventricular pressure continues to rise as the contraction increases its force
(red line) – then starts to decrease as blood begins to be ejected
• at the end of the systole there is a small volume of blood that remains in the
ventricle – end-systole volume (ESV), 65ml (15)
• EDV-ESV = SV (point 7 – point 15)
• G. Ventricular repolarization
• T wave – point 16
• as the ventricle relaxes – ventricular pressure falls below aortic and the aortic SL
closes (17)
• this closure produces a small disturbance in the aortic pressure curve – dicrotic
notch (18)

48. • H. Isovolumetric ventricular relaxation – Start of Ventricular
Diastole
• all valves are closed because ventricular pressure still
exceeds atrial pressure – isovolumetric relaxation (19)
• chamber volume remains constant (20)
• I. Ventricular filling/MidVentricular Diastole
• as VP falls below AP – the AV valve opens again (21) and
ventricular filling starts again increasing ventricular
volume (blue line)
• as the atria fills from blood from the pulmonary veins
(lungs) it increases AP
• with the AV valve open this blood fills the ventricle
rapidly (23)
• then slows down (24) as the blood drains the atrium
• during this period of reduced filling, blood continues to
come in from the pulmonary veins – goes directly into
the ventricle
• cycle starts again with a new SA depolarization
Cardiac cycle

49. Heart Sounds
• Closing of the AV and
semilunar valves.
• Lub (first sound):
• Produced by closing of the AV
valves during isovolumetric
contraction.
• Dub (second sound):
• Produced by closing of the
semilunar valves when
pressure in the ventricles falls
below pressure in the
arteries.